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Vascular endothelial function is improved after active mattress use
Journal of Wound Care
Abstract
Objective
Active mattresses are used to prevent, treat and relieve pressure ulcers (PU) by intermittent contact pressure/relief. However, no studies have directly assessed the vascular endothelial response to long-term active mattress use. This study investigated the hypothesis that eight weeks use of an active mattress would lead to improvements in vascular endothelial function in healthy participants.
Methods
Physiological parameters of baseline skin temperature (BskT), resting blood flow (RBF) and endothelial function as measured using post-occlusive reactive hyperaemia (PORH), were assessed at baseline (week 0); following eight weeks of sleeping on an active mattress, and after an eight week washout period (at week 16).
Results
We recruited 10 healthy participants (four male, age 52.7±8.5 years, six female age 51.8±17.5 years). Following active mattress use RBF, PORH and BskT at the hallux pulp increased by 336%, 197% and 3.5ºC, respectively. Mean values increased from 24.3±38.3 perfusion units to 106.0±100.3 perfusion units (p=0.021) and from 13,456±10,225 to 40,252±23,995 perfusion units x seconds (p=0.003) and from 22.9±2.5ºC to 26.4±1.9ºC (p<0.001), respectively.
Conclusion
Active mattress use for eight weeks leads to significant improvements in RBF, PORH, and BskT. These results suggest that active mattress use can improve endothelial function. Future research is required to explore the potential of active mattress use in the treatment and management of diseases and conditions that would benefit from an improved endothelial function.
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Background
We sought to determine the effects of unilateral lower-limb external pneumatic compression (EPC) on bilateral lower-limb vascular reactivity and skin blood flow.
Methods
Thirty-two participants completed this two-aim study. In AIM1 (n = 18, age: 25.5 ± 4.7 years; BMI: 25.6 ± 3.5 kg/m²), bilateral femoral artery blood flow and reactivity (flow mediated dilation [FMD]) measurements were performed via ultrasonography at baseline (PRE) and immediately following 30-min of unilateral EPC treatment (POST). AIM2 (n = 14, age: 25.9 ± 4.5; BMI: 27.2 ± 2.7 kg/m²) involved 30-min unilateral EPC (n = 7) or sham (n = 7) treatment with thermographic bilateral lower-limb mean skin temperature (MST) measurements at baseline, 15-min of treatment (T15) and 0, 30 and 60-min (R0, R30, R60) following treatment.
Results
Comparative data herein are presented as mean ± 95% confidence interval. AIM1: No significant effects on total reactive hyperemia blood flow were observed for the treated (i.e., compressed) or untreated (i.e., non-compressed) leg. A significant effect of time, but no time*leg interaction, was observed for relative FMD indicating higher reactivity bilaterally with unilateral EPC treatment (FMD: +0.41 ± 0.09% across both legs; p < 0.05). AIM2: Unilateral EPC treatment was associated with significant increases in whole-leg MST from baseline during (T15: +0.63 ± 0.56 °C in the visible untreated/contralateral leg, p < 0.025) and immediately following treatment (i.e., R0) in both treated (+1.53 ± 0.59 °C) and untreated (+0.60 ± 0.45 °C) legs (p < 0.0125). Across both legs, MST remained elevated with EPC at 30-min post-treatment (+0.60 ± 0.45 °C; p < 0.0167) but not at 60-min post (+0.27 ± 0.46 °C; p = 0.165). Sham treatment was associated with a significant increase in the treated leg immediately post-treatment (+1.12 ± 0.31 °C; p < 0.0167), but not in the untreated leg (−0.27 ± 0.12 °C). MST in neither the treated or untreated leg were increased relative to baseline at R30 or R60 (p > 0.05). Finally, during treatment and at all post-treatment time points (i.e., R0, R30 and R60), independent of treatment group (EPC vs. sham), there was a significant effect of region. The maximum increase in MST was observed at the R0 time point and was significantly (p < 0.05) larger in the thigh region (+1.02 ± 0.31 °C) than the lower-leg (+0.47 ± 0.29 °C) region. However, similar rates of MST decline from R0 in the thigh and lower leg regions were observed at the R30 and R60 time points.
Discussion
Unilateral EPC may be an effective intervention for increasing skin blood flow and/or peripheral conduit vascular reactivity in the contralateral limb. While EPC was effective in increasing whole-leg MST bilaterally, there appeared to be a more robust response in the thigh compared to the lower-leg. Thus, proximity along the leg may be an important consideration in prospective treatment strategies.
The aim was to assess endothelial function with photoplethysmography (PPG), by post-occlusive reactive hyperaemia (PORH) combined with alprostadil challenge test in patients with peripheral artery disease (PAD).
: Forty-nine PAD patients stage II-III Fontaine (39 male, 10 female, mean age 68.45±5.86 years) and a control group of 49 healthy individuals (24 male, 25 female; mean age 25.1±3.8 for a young subgroup; 71.0±0.16 years for an elderly subgroup) were included. Ankle-brachial index (ABI) was assessed at baseline, peripheral perfusion (PP) and PORH were assessed at baseline and after the 30 minutes administration of parenteral alprostadil.
: After 3 minutes of arterial occlusion, peripheral perfusion increased from 0.69±0.94 mV/V to 2.27±2.42 mV/V (p<0.0001). After alprostadil challenge, peripheral perfusion increased from 0.84±1.24 mV/V to 4.52±3.52 mV/V (p<0.0001). In controls PP was 2.4±1.7 mV/V versus 3.8±1.5 mV/V, p<0.0001.
: In patients with PAD, an increase in PORH after alprostadil challenge due to the release of nitric oxide (NO), provides information on the endothelial function and could reflect the presence of collaterals. In the healthy control group, the increase in PORH could reflect the integrity of main arterial branch. In PAD patients with an increase in PORH, conservative therapy should be preferred over surgical revascularisation.
Objective
This study examined whether the presence of peripheral sensory neuropathy or cardiac autonomic deficits is associated with postocclusive reactive hyperemia (reflective of microvascular function) in the diabetic foot.
Research design and methods
99 participants with type 2 diabetes were recruited into this cross-sectional study. The presence of peripheral sensory neuropathy was determined with standard clinical tests and cardiac autonomic function was assessed with heart rate variation testing. Postocclusive reactive hyperemia was measured with laser Doppler in the hallux. Multiple hierarchical regression was performed to examine relationships between neuropathy and the peak perfusion following occlusion and the time to reach this peak.
Results
Peripheral sensory neuropathy predicted 22% of the variance in time to peak following occlusion (p<0.05), being associated with a slower time to peak but was not associated with the magnitude of the peak. Heart rate variation was not associated with the postocclusive reactive hyperemia response.
Conclusions
This study found an association between the presence of peripheral sensory neuropathy in people with diabetes and altered microvascular reactivity in the lower limb.
Background
The aim of the present study was to evaluate changes in microvascular density and reactivity in patients with type 1 diabetes (T1D) resulting from low intensity chronic exercise training. Methods
This study included 22 (34 ± 7 years) consecutive outpatients with T1D and disease duration > 6 years. We used intravital video-microscopy to measure basal skin capillary density and capillary recruitment using post-occlusive reactive hyperemia (PORH) in the dorsum of the fingers. Endothelium-dependent and -independent vasodilation of the skin microcirculation was evaluated in the forearm with a laser Doppler flow monitoring (LDF) system in combination with acetylcholine and sodium nitroprusside iontophoresis, PORH and local thermal hyperemia. ResultsThe basal mean capillary density (MCD) after exercise training was significantly higher than before exercise (134 ± 25 vs. 119 ± 19 capillaries/mm2, respectively; P = 0.0013). MCD during PORH was also higher after exercise (140 ± 26 vs. 121 ± 24 capillaries/mm2, respectively; P < 0.0001). Endothelium-dependent capillary recruitment during PORH was also significantly higher after exercise (140 ± 26 vs. 134 ± 25 capillaries/mm2, respectively; P < 0.0012). There were no significant changes in skin microvascular reactivity after exercise as investigated using LDF. Conclusions
Our results showed that low intensity aerobic exercise, performed four times per week for 12 weeks by patients with T1D, induces significant increases in microvascular density and endothelial-dependent capillary reactivity. Trial registrationClinicalTrials.gov NCT02441504. Registered 7 May 2015.
Background
In patients with chronic leg ischemia, the beneficial effect of arterial revascularization can be significantly decreased due to postoperative leg swelling. The aim of this study was to assess the effects of intermittent pneumatic compression (IPC) on skin flow normalization in patients undergoing revascularization procedures due to chronic leg ischemia.
Material/Methods
We evaluated 116 patients with chronic leg ischemia. The patients were divided into groups according to the performed treatment (endovascular or surgical) and implementation of IPC postoperatively. The leg edema assessment and microcirculation flow assessment were performed pre- and postoperatively, using percutaneous O2 pressure (TcpO2), cutaneous blood perfusion (CBP) measurements, and skin flow motion assessment.
Results
In patients who did not receive IPC, a decrease in CBP value was observed in the 1st postoperative assessment. Among patients receiving IPC, the CBD value increased at the 1st and 2nd postoperative measurements, especially in the surgical group. The lowest TcpO2 values were observed in by-pass surgery group without IPC postoperatively.
Conclusions
The benefits of the by-pass procedure in patients with leg ischemia can be significantly reduced by postoperative edema. Among patients with postoperative leg edema, local tissue blood perfusion can be improved by the use of IPC, which can result in decreased local leg swelling, as well as improved skin blood perfusion and TcpO2.
The endothelium, by area alone, is one of the largest organs in the body comprised of up to trillion cells, weighing over 1 kg, and covering nearly 3 m2 in a 70 kg male.1,2 Moreover, it interacts with nearly every system in the body, and has been implicated in end organ diseases of systems such as neurologic, renal, hepatic, vascular, dermatologic, immunologic, and of course cardiac. The endothelium is a single vessel layer standing as the ultimate layer between blood and vascular supply to other tissues, and serving multiple purposes. The first and foremost is a hemostatic balance between thrombosis and anticoagulation via a careful series of checks and balances discussed below. Additionally, the endothelium regulates vascular tone, carefully balancing vasoconstriction and vasodilation to provide adequate perfusion pressure to target organs. Other functions include regulation of angiogenesis, wound healing, smooth muscle cell proliferation, fibrosis, and inflammation. Factors that adversely affect the endothelium include common cardiovascular risk factors such as tobacco use, obesity, age, hypertension, hyperlipidemia, physical inactivity, and poor dietary habits. Alternatively, factors that positively impact the function of the endothelium are, essentially, beneficial lifestyle habits opposite to those mentioned above such as increased physical activity, dietary habits which include anti-inflammatory and anti-oxidant foods, and some pharmaceutical agents such as L-Arginine.
Presently there is no guideline directive – either pro or con – to routinely include endothelial function testing in cardiovascular disease (CVD) risk assessment.3–5
Exercise is a powerful therapy for preventing the onset of and slowing the progression of cardiovascular disease. Increased shear stress during exercise improves vascular homeostasis by both decreasing reactive oxygen species and increasing nitric oxide bioavailability in the endothelium. While these observations are well accepted as they apply to individuals at risk for cardiovascular disease, less is known about how exercise, especially intense exercise, affects vascular function in healthy individuals. This review highlights examples of how vascular function can paradoxically be impaired in otherwise healthy individuals by extreme levels of exercise, with a focus on the causative role that reactive oxygen species play in this impairment.
Objective
To determine if lower extremity exercise-induced muscle injury (EMI) reduces vascular endothelial function of the upper extremity and if massage therapy (MT) improves peripheral vascular function after EMI.
Design
Randomized, blinded trial with evaluations at 90 minutes, 24 hours, 48 hours, and 72 hours.
Setting
Clinical research center at an academic medical center and laboratory
Participants
Thirty-six sedentary young adults were randomly assigned to one of three groups: 1) EMI + MT (n=15; mean age ± standard error (SE): 26.6±0.3), 2) EMI only (n=10; mean age ± SE: 23.6±0.4), and 3) MT only (n=11; mean age ± SE: 25.5 ± 0.4).
Intervention
Participants were assigned to either EMI only (a single bout of bilateral, eccentric leg-press exercise), MT only (30-minute lower extremity massage using Swedish technique), or EMI + MT.
Main outcome measures
Brachial artery flow-mediated dilation (FMD) was determined by ultrasound at each time point. Nitroglycerin-induced dilation was also assessed (NTG; 0.4 mg).
Results
Brachial FMD increased from baseline in the EMI + MT group and the MT only group (7.38±0.18 to 9.02±0.28%, p<0.05 and 7.77±0.25 to 10.20±0.22%, p < 0.05, respectively) at 90 minutes remaining elevated until 72 hrs. In the EMI only group FMD was reduced from baseline at 24 and 48 hrs (7.78±0.14 to 6.75±0.11%, p<0.05 and 6.53±0.11, p<0.05, respectively) returning to baseline after 72 hrs. Dilations to NTG were similar over time.
Conclusions
Our results suggest that MT attenuates impairment of upper extremity endothelial function resulting from lower extremity EMI in sedentary young adults.
Uraemia and hypertension are associated with higher risk for cardiovascular complications. Endothelial dysfunction plays an important role in the pathogenesis of cardiovascular diseases. The aim of the present study was to evaluate endothelial function in the forearm skin microcirculation of patients with essential hypertension, in hypertensive haemodialysis patients and in normotensive control subjects.
We performed laser Doppler flowmetry with iontophoresis of acetylcholine (ACh) and of sodium nitroprusside (SNP) as well as the post-occlusive reactive hyperaemia test (PORH) in 16 normal control subjects (CONT), in 16 patients with essential hypertension (EHT) and in 16 haemodialysis patients with essential hypertension (DHT). Plasma levels of endothelin-1, big-endothelin and von Willebrand factor (vWF) were also measured.
The average hyperaemic response to the higher dose of ACh iontophoresis was 801+/-110% in CONT, 563+/-69 % in EHT and 308+/-64% in DHT (P<0.05, between all comparisons). Vasodilation to the higher dose of SNP was 791+/-79% in CONT, 633+/-72% in EHT and 355+/-69% in DHT (NS, P<0.001 compared with controls, respectively). The average peak flow during PORH was significantly lower in both the EHT and DHT groups compared with controls (294+/-39, 267+/-59 and 429+/-45%, respectively, P<0.05). Levels of endothelin-1, big endothelin, vWF and vWF activity were significantly higher in the DHT group (P<0.05, compared with controls).
In hypertensive haemodialysis patients, both endothelium-dependent and -independent vasodilation was impaired. The observed increase in plasma markers of endothelial damage indicated a progression of vascular disease.
We undertook this study to determine whether long-term high intensity exercise would modify cutaneous endothelial-dependent vasodilation. We compared a group of 9 highly trained windsurfers (mean age: 24.5 +/- 1.6 years) to a control group of 8 sedentary individuals (22.9 +/- 0.4 years, NS). Laser Doppler was used to measure cutaneous blood flow in the resting state (baseline), during post-occlusive hyperaemia (endothelium-dependent vasodilation), and local heating to 42 degrees C. Lipid profile was similar in both groups. Resting heart rate was significantly lower in windsurfers. Baseline cutaneous vascular conductance (CVC) values were similar in both groups (0.059 +/- 0.016 and 0.051 +/- 0.009). During reactive hyperaemia, normalized peak CVC value was significantly higher in the windsurfers group (1775.4 +/- 286.9 and 826.4 +/- 121.7 % baseline CVC; p = 0.01). Normalized peak CVC value in response to local heating (42 degrees C) was not significantly different between both groups (2359.4 +/- 346.1 and 1467.7 +/- 282.6 % baseline CVC). Endothelium-dependent vasodilation in cutaneous microcirculation is significantly enhanced in the forearm skin of highly trained windsurfers when compared to sedentary controls.
Atherosclerosis is a disease of blood vessel walls that is thought to be initiated as a reaction of insults to the endothelium. The complex sequence of cellular events that begins with focal inflammation leads to the accumulation of leukocytes in the subendothelial layer and unrestricted uptake of oxidized lipoproteins by macrophages and smooth muscle cells, leading to foam cell formation. Vascular endothelial cells do not undergo the foam cell transformation and do not accumulate cholesterol in atherosclerotic plaques to the same extent as macrophages or smooth muscle cells. However, vascular endothelial cells express receptors for oxidized lipoproteins, and have the biochemical pathways for sterol synthesis and receptor-mediated endocytosis of lipoproteins. Data from the authors' laboratory show that high density lipoproteins but not lipid-free apolipoprotein A-I promote cellular cholesterol efflux in human umbilical vascular endothelial cells and human aortic endothelial cells. Gene expression microarrays were used to examine the differential expression of genes after cholesterol loading. While sterol regulatory element-binding protein-sensitive genes were downregulated, the authors identified a novel transporter, the ATP-binding cassette G1 (ABCG1) to be highly expressed in response to both cellular cholesterol loading and stimulation with the liver X receptor agonist 22-hydroxycholesterol. The ABCA1 gene and protein, the major modulator of cellular cholesterol efflux in macrophages and in peripheral and hepatic tissues, are only weakly expressed in human umbilical vascular endothelial cells and human aortic endothelial cells. These data suggest that endothelial cells maintain cholesterol homeostasis by downregulating cholesterol synthesis and low density lipoprotein receptors and by a cellular cholesterol efflux mechanism onto low-affinity but high-capacity high density lipoproteins. The role of ABC-type transporters, including ABCG1, requires further examination.
The vascular endothelium constitutes approximately 1% of body mass (1kg) and has a surface area of approximately 5000m(2). The endothelium is a multifunctional endocrine organ strategically placed between the vessel wall and the circulating blood, and has a key role in vascular homeostasis. The endothelium is both a target for and mediator of cardiovascular disease. The endothelium releases several relaxing and constricting factors, which can affect vascular homeostasis. Endothelial dysfunction, whether caused by physical injury or cellular damage, leads to compensatory responses that alter the normal homeostatic properties of the endothelium. In this review, we summarized some physiological aspects of endothelial function and then we discussed endothelial dysfunction during some pathological conditions.
Current methods of fracture care use various adjuncts to try and decrease time to fracture union, improve fracture union rates and enhance functional recovery. Intermittent pneumatic compression (IPC), one such modality, is used in the management of both fractures and soft-tissue injuries.
A search of PubMed, Medline, CINAHL, DH data and Embase databases was performed using the following keywords 'intermittent pneumatic compression', 'fracture healing' and 'soft tissue healing'. Sixteen studies on the use of IPC in fracture and soft-tissue healing were identified. These studies demonstrated that IPC facilitates both fracture and soft-tissue healing with rapid functional recovery.
IPC appears to be an effective modality to enhance fracture and soft-tissue healing. However, the number of subjects in human studies is small, and adequately powered randomized controlled trials in humans are required to produce stronger clinically relevant evidence.
Vascular impairment, a main feature of the pathogenesis of systemic sclerosis (SSc), involves both the macro- and the microvasculature. We compared and correlated simultaneously measured skin microvascular and brachial artery macrovascular post-occlusive hyperemia in 3 groups: patients with SSc, patients with primary Raynaud's phenomenon (RP), and healthy volunteers.
Thirty-three healthy volunteers, 36 patients with primary RP, and 42 patients with SSc were enrolled. For each subject, brachial artery flow-mediated dilation (FMD) and cutaneous post-occlusive reactive hyperemia (PORH) were simultaneously recorded after 5-minute occlusion of the brachial artery. Local thermal hyperemia, nitroglycerin-mediated dilation (NMD), intima-media thickness (IMT), and pulse wave velocity (PWV) were also assessed.
Digital cutaneous peak PORH was altered in patients with primary RP and SSc compared to healthy controls, whereas FMD was not significantly different among all groups. We observed a correlation between digital peak cutaneous vascular conductance and brachial FMD in healthy controls (r = 0.49; p = 0.004), but not in patients with primary RP or SSc. Thermal hyperemia was altered only in patients with SSc. Brachial NMD, IMT, and PWV were not different among all groups.
We observed a loss of the correlation between brachial FMD and digital cutaneous PORH in patients with SSc and primary RP. Microvascular function is impaired in SSc, whereas brachial artery endothelial function is normal.
Flow-mediated dilatation (FMD) is an established, but investigator-demanding method, used to non-invasively determine nitric oxide (NO)-dependent endothelial function in humans. Local thermal hyperemia (LTH) or post-occlusive reactive hyperemia (PORH) of the skin measured with a laser Doppler flow imager may be a less demanding alternative of FMD. We investigated the reproducibility of the different measures of vascular function, their interrelationship and the NO-dependency of LTH. Measurements were performed twice in 27 healthy men (8 smokers), one week apart. Local application of NG-monomethyl-l-arginine (L-NMMA) by means of iontophoresis was used to determine the NO-dependency of LTH. Using L-NMMA, the peak and plateau responses of LTH were reduced by 31% (p < .001) and 65% (<0.001), respectively. For all measurements the coefficient of variation (CV) was higher in smokers than in non-smokers. For non-smokers the CV of FMD was 12%, of LTH peak response 17%, of LTH plateau response 12%, of PORH peak response 14% and of PORH area under the curve response 11%. FMD correlated weakly with the PORH peak and area under the curve response (r = 0.39 and 0.43, p < .05), whereas the LTH-plateau response correlated with the PORH peak response (r = 0.68, p < .01) in non-smokers, but FMD and LTH peak or plateau responses were unrelated. In conclusion, the LTH plateau response is for two-third NO-dependent, but unrelated to FMD. Furthermore, despite easy to perform the LTH responses are not more reproducible than FMD. Given the weak associations, the different methods of vascular function assessment are not interchangeable.
Materials and methods:
Eighteen of these patients received treatment with high-pressure, intermittent pneumatic compression (HPIPC) 60 minutes twice daily for 16 weeks, and 16 subjects received standard care consisting of an exercise regimen of walking for 20 minutes twice daily for 16 weeks. The HPIPC device delivers bilateral pressures of 120 mm Hg. Cycle times provide sequential compression for 4 seconds (+/- 0.5 seconds) followed by a 16-second rest period (+/- 3.0 seconds), resulting in a 20-second cycle or 3 cycles per minute. The study was designed to measure patient-centered outcomes. The primary endpoint was peak walking time (PWT), defined as time to maximally tolerated claudication pain. Secondary endpoints included change in resting ankle brachial index, ulcer healing, relief of resting/wound pain, and quality of life (QoL) index. Age (73.7 years vs 72.7 years), baseline PWTs (1-6 minutes), and risk factors were similar in both treatment groups.
Results:
At 4 weeks, the percent change from baseline in PWT did not vary significantly between treatment groups (17.8% for HPIPC and 17% for standard care). After 8 weeks, the percent change in PWT for the HPIPC group was 41% compared to 32% for the group receiving standard care (P = 0.062). At the 16-week time point the percent change from baseline in PWT was significantly different between treatment arms (35.5% for the standard care group and 54.7% for the group receiving HPIPC [P = 0.043]). The mean reduction in wound surface area was 57% and 71% at 12 weeks and 16 weeks, respectively, for the HPIPC group, compared to 45% and 56% for the control group. The HPIPC group reported significantly greater pain relief at the 12-week (P = 0.044) and 16- week (P = 0.038) time points. Compared to the control group, the HPIPC group reported improvement in patient-centered outcomes such as physical function and bodily pain. These differences were statistically significant (P less than 0.05) at the 16- week evaluation period.
Conclusion:
Therapy consisting of HPIPC for 2 hours daily for a period of 16 weeks significantly improved PWT, reduced resting pain, and improved healing rates, physical function, and bodily pain. There were no devicerelated complications, allowing for long-term use. This study further supports that HPIPC is safe and effective and should be considered for patients who are not candidates for endovascular or surgical procedures. Furthermore, HPIPC offers an excellent alternative for the palliative care of patients with PAD and CLI symptoms.
Objective:
The aim of this study was to explore the interaction between interface pressure, pressure-induced vasodilation, and reactive hyperaemia with different pressure-redistribution mattresses.
Method:
A cross-sectional study was performed with a convenience sample of healthy young individuals, and healthy older individuals and inpatients, at a university hospital in Sweden. Blood flow was measured at depths of 1mm, 2mm, and 10mm using laser Doppler flowmetry and photoplethysmography. The blood flow, interface pressure and skin temperature were measured in the sacral tissue before, during, and after load while lying on one standard hospital mattress and three different pressure-redistribution mattresses.
Results:
There were significant differences between the average sacral pressure, peak sacral pressure, and local probe pressure on the three pressure-redistribution mattresses, the lowest values found were with the visco-elastic foam/air mattress (23.5 ± 2.5mmHg, 49.3 ± 11.1mmHg, 29.2 ± 14.0mmHg, respectively). Blood flow, measured as pressure-induced vasodilation, was most affected in the visco-elastic foam/air group compared to the alternating pressure mattress group at tissue depths of 2mm (39.0% and 20.0%, respectively), and 10mm (56.9 % and 35.1%, respectively). Subjects in all three groups, including healthy 18-65 year olds, were identified with no pressure-induced vasodilation or reactive hyperaemia on any mattress (n=11), which is considered a high-risk blood flow response.
Conclusion:
Interface pressure magnitudes considered not harmful during pressure-exposure on different pressure-redistribution mattresses can affect the microcirculation in different tissue structures. Despite having the lowest pressure values compared with the other mattresses, the visco-elastic foam/air mattress had the highest proportion of subjects with decreased blood flow. Healthy young individuals were identified with the high-risk blood flow response, suggesting an innate vulnerability to pressure exposure. Furthermore, the evaluation of pressure-redistribution support surfaces in terms of mean blood flow during and after tissue exposure is not feasible, but assessment of pressure-induced vasodilation and reactive hyperaemia could be a new way to assess individualised physiological measurements of mechanisms known to be related to pressure ulcer development.
Although the entire coronary tree is exposed to the atherogenic effect of the systemic risk factors, atherosclerotic lesions form at specific arterial regions, where low and oscillatory endothelial shear stress (ESS) occur. Low ESS modulates endothelial gene expression through complex mechanoreception and mechanotransduction processes, inducing an atherogenic endothelial phenotype and formation of an early atherosclerotic plaque. Each early plaque exhibits an individual natural history of progression, regression, or stabilization, which is dependent not only on the formation and progression of atherosclerosis but also on the vascular remodeling response. Although the pathophysiologic mechanisms involved in the remodeling of the atherosclerotic wall are incompletely understood, the dynamic interplay between local hemodynamic milieu, low ESS in particular, and the biology of the wall is likely to be important. In this review, we explore the molecular, cellular, and vascular processes supporting the role of low ESS in the natural history of coronary atherosclerosis and vascular remodeling and indicate likely mechanisms concerning the different natural history trajectories of individual coronary lesions. Atherosclerotic plaques associated with excessive expansive remodeling evolve to high-risk plaques, because low ESS conditions persist, thereby promoting continued local lipid accumulation, inflammation, oxidative stress, matrix breakdown, and eventually further plaque progression and excessive expansive remodeling. An enhanced understanding of the pathobiologic processes responsible for atherosclerosis and vascular remodeling might allow for early identification of a high-risk coronary plaque and thereby provide a rationale for innovative diagnostic and/or therapeutic strategies for the management of coronary patients and prevention of acute coronary syndromes.
Background
Pressure ulcers are associated with severe impairment for the patients and high economic load. With this study we wanted to gain more insight to the skin perfusion dynamics due to external loading. Furthermore, we evaluated the effect of different types of pressure relief mattresses.
Methods
A total of 25 healthy volunteers were enrolled in the study. Perfusion dynamics of the sacral and the heel area were assessed using the O2C-device, which combines a laser light, to determine blood flow, and white light to determine the relative amount of hemoglobin. Three mattresses were evaluated compared to a hard surface: a standard hospital foam mattress bed, a visco-elastic foam mattress, and an air-fluidized bed.
Results
In the heel area, only the air-fluidized bed was able to maintain the blood circulation (mean blood flow of 13.6 ± 6 versus 3.9 ± 3 AU and mean relative amount of hemoglobin of 44.0 ± 14 versus 32.7 ± 12 AU.) In the sacral area, all used mattresses revealed an improvement of blood circulation compared to the hard surface.
Conclusion
:The results of this study form a more precise pattern of perfusion changes due to external loading on various pressure relief mattresses. This knowledge may reduce the incidence of pressure ulcers and may be an influencing factor in anti-decibitus mattress selection.
The glycocalyx is a dynamic network of multiple membrane-bound complexes lining the vascular endothelium. Its role in maintaining vascular homeostasis includes regulating vascular permeability as well as a range of vital functions, such as mechanotransduction, hemostasis, modulation of inflammatory processes, and serving as an antiatherogenic. Revisionist thinking about the Starling principle is discussed in terms of the major influence of the glycocalyx on capillary and tissue fluid homeostasis. The clinical and pathophysiologic threats to the glycocalyx are reviewed as well as strategies to maintain its integrity.
Pressure ulcers in spinal cord injury represent a challenging problem for patients, their caregivers, and their physicians. They often lead to recurrent hospitalizations, multiple surgeries, and potentially devastating complications. They present a significant cost to the healthcare system, they require a multidisciplinary team approach to manage well, and outcomes directly depend on patients' education, prevention, and compliance with conservative and surgical protocols. With so many factors involved in the successful treatment of pressure ulcers, an update on their comprehensive management in spinal cord injury is warranted. Current concepts of local wound care, surgical options, as well as future trends from the latest wound healing research are reviewed to aid medical professionals in treating patients with this difficult problem.
The mechanisms by which intermittent pneumatic leg compression (IPC) treatment effectively treats symptoms associated with peripheral artery disease remain speculative. With the aim of gaining mechanistic insight into IPC treatment, the purpose of this study was to investigate the effect of IPC frequency on limb hemodynamics, vascular function, and skeletal muscle gene expression. In this two study investigation, healthy male subjects underwent an hour of either high-frequency (HF; 2-s inflation/3-s deflation) or low-frequency (LF; 4-s inflation/16-s deflation) IPC treatment of the foot and calf. In study 1 (n = 11; 23.5 ± 4.7 yr), subjects underwent both HF and LF treatment on separate days. Doppler/ultrasonography was used to measure popliteal artery diameter and blood velocity at baseline and during IPC treatment. Flow-mediated dilation (FMD) and peak reactive hyperemia blood flow (RHBF) were determined before and after IPC treatment. In study 2 (n = 19; 22.0 ± 4.6 yr), skeletal muscle biopsies were taken from the lateral gastrocnemius of the treated and control limb at baseline and at 30- and 150-min posttreatment. Quantitative PCR was used to assess mRNA concentrations of genes associated with inflammation and vascular remodeling. No treatment effect on vascular function was observed. Cuff deflation resulted in increased blood flow (BF) and shear rate (SR) in both treatments at the onset of treatment compared with baseline (P < 0.01). BF and SR significantly diminished by 45 min of HF treatment only (P < 0.01). Both treatments reduced BF and SR and elevated oscillatory shear index compared with baseline (P < 0.01) during cuff inflation. IPC decreased the mRNA expression of cysteine-rich protein 61 from baseline and controls (P <0 .01) and connective tissue growth factor from baseline (P < 0.05) in a frequency-dependent manner. In conclusion, a single session of IPC acutely impacts limb hemodynamics and skeletal muscle gene expression in a frequency-dependent manner but does not impact vascular function.
The aim of this study was to compare cutaneous microvascular function in young healthy subjects (n=50) with that of cardiometabolic diseased patients (n=50) using laser speckle contrast imaging (LSCI) coupled with transdermal iontophoretic delivery of acetylcholine (ACh) and post-occlusive reactive hyperemia (PORH).
Cutaneous blood flow was assessed in the forearm using LSCI at rest, during PORH and during iontophoresis of ACh with increasing anodal currents of 30, 60, 90, 120, 150 and 180 μA during 10-second intervals spaced 1 min apart.
Endothelium-dependent skin microvascular vasodilator responses induced by both ACh and PORH were significantly reduced in cardiometabolic diseased patients compared to healthy subjects. Vasodilator responses induced by ACh were significantly higher in young women than in young men. Iontophoresis charges up to 1.5 mC do not induce nonspecific effects on skin microvascular flux.
LSCI appears to be a promising noninvasive technique for evaluating systemic microvascular endothelial function.
Laser Doppler fluxmetry (LDF) can non-invasively measure skin microvascular changes in response to acetylcholine (ACh), local heating of the skin and reactive hyperaemia following arterial occlusion. Various studies have used microvascular changes in response to these stimuli, especially ACh iontophoresis and local heating, as a surrogate marker of endothelial function. There are few data in the literature regarding the comparative reproducibility of microvascular perfusion changes induced by the three stimuli. The aim of this study was to systematically assess and compare the reproducibility of skin microcirculatory function in response to each of these challenges. Ten healthy non-smoking subjects (seven males) median age 36 years (range 23-46), with no history of hypertension, diabetes, coronary artery disease or any connective tissue disorder, were studied. Changes in skin microcirculation in response to ACh iontophoresis, local heating of the skin and post-occlusive reactive hyperaemia, on two separate days (median 31, range 11-42 days), were assessed in all subjects. We measured three parameters: the change in perfusion from baseline perfusion (peak minus baseline perfusion), the relative percentage change in perfusion from baseline (peak--baseline)/baseline x 100 (%) and also the time-to-peak perfusion. The reproducibility of the change in perfusion had coefficients of variation (CV) of 9.3% for local skin heating, 19.4% for reactive hyperaemia and 25.5% for ACh iontophoresis. The relative percentage change in perfusion from baseline was more variable with CVs ranging from 23% to 39%. The coefficient of variation of time-to-peak perfusion was 7.0% for heating, 15.1% for reactive hyperaemia and 10.4% for ACh iontophoresis. We have shown that microcirculatory changes measured by the change in perfusion from baseline and time-to-peak perfusion in response to ACh, post-occlusive reactive hyperaemia and local skin heating had good reproducibility when carried out in a controlled environment with a standardized protocol. Relative change in perfusion had relatively poor reproducibility. The change in perfusion and time-to-peak perfusion for local skin heating were the most reproducible overall.
Age-related increases in oxidative stress impair endothelium-dependent vasodilatation in humans, leading to the speculation that endothelial dysfunction contributes to impaired muscle blood flow and vascular control during exercise in older adults. We directly tested this hypothesis in 14 young (22 +/- 1 years) and 14 healthy older men and women (65 +/- 2 years). We measured forearm blood flow (FBF; Doppler ultrasound) and calculated vascular conductance (FVC) responses to single muscle contractions at 10, 20 and 40% maximum voluntary contraction (MVC) before and during ascorbic acid (AA) infusion, and we also determined the effects of AA on muscle blood flow during mild (10% MVC) continuous rhythmic handgrip exercise. For single contractions, the peak rapid hyperaemic responses to all contraction intensities were impaired approximately 45% in the older adults (all P < 0.05), and AA infusion did not impact the responses in either age group. For the rhythmic exercise trial, FBF (approximately 28%) and FVC (approximately 31%) were lower (P = 0.06 and 0.05) in older versus young adults after 5 min of steady-state exercise with saline. Subsequently, AA was infused via brachial artery catheter for 10 min during continued exercise. AA administration did not significantly influence FBF or FVC in young adults (1-3%; P = 0.24-0.59), whereas FBF increased 34 +/- 7% in older adults at end-exercise, and this was due to an increase in FVC (32 +/- 7%; both P < 0.05). This increase in FBF and FVC during exercise in older adults was associated with improvements in vasodilator responses to acetylcholine (ACh; endothelium dependent) but not sodium nitroprusside (SNP; endothelium independent). AA had no effect on ACh or SNP responses in the young. We conclude that acute AA administration does not impact the observed age-related impairment in the rapid hyperaemic response to brief muscle contractions in humans; however, it does significantly increase muscle blood flow during continuous dynamic exercise in older adults, and this is probably due (in part) to an improvement in endothelium-dependent vasodilatation.
Conventional paraplegic nursing is based on ‘skin care’ only, i.e. 2 or 3 hourly turning on a soft bed. This gives the absolute minimum protection. Body weight acts through the skeleton, and is transferred to a natural hard surface, via wieght bearing bony prominences, which protect vital tissues from ischaemia. This is not so on a soft surface where pressure causes ischaemia of muscle. There is evidence that 20 minutes ischaemia injures muscle. Injured muscle can repair itself. The majority of decubitus lesions therefore go undetected. There is proof that ischaemic muscle necrosis occurs well before skin necrosis. Therefore the prevention of decubiti on the European bed should be based on ‘muscle care’. Normal sleeping subjects make on average, one gross postural change every 11.6 minutes. It is postulated that this is the minimum physiological mobility requirement for man supported on a soft surface. The physiological gross postural change was determined by observing man sleeping on the ground. Excluding the prone position, the fully lateral, with lower limbs flexed, or the supine, are the only stable sleeping postures. Considering these and many other factors, the optimum nursing condition was determined, i.e. kinetic nursing, which is by definition: the automatic and continuous turning of a patient equally from side to side, in a given posture, through a maximum excursion of 124° at a minimum rate of 124° in 4.5 minutes. The Roto Rest beds are a practical means of providing this.
The increase in venous pressure during leg dependency causes a vasoconstriction of the distal vascular bed in healthy subjects, which is due to the so-called veno-arteriolar reflex. The aim of the present study was to investigate if this reflex is disturbed in patients with severe peripheral arterial occlusive disease (PAOD), with and without diabetes. The total skin microcirculation during rest and postocclusive reactive hyperemia (PRH) after a three minute arterial occlusion at the ankle was studied by laser Doppler (LD) fluxmetry. The LD probe was attached to the dorsal region of the foot in 10 legs of healthy control subjects, patients with PAOD, and patients with PAOD and diabetes respectively. No vasoconstriction was seen in the PAOD group when the leg was moved from the supine to the dependent position. The PRH response was also significantly (p less than 0.05-0.01) impaired compared to the controls in both positions. The diabetic PAOD patients had an almost normal reactivity in spite of an equally reduced arterial circulation as the non-diabetic patients. The results show that patients with PAOD have a significantly disturbed reactivity of the skin microcirculation in the ischemic foot, while the reactivity in diabetic PAOD patients is almost normal.
Skin-surface temperature gradients (forearm temperature - fingertip temperature) have been used as an index of thermoregulatory peripheral vasoconstriction. However, they have not been specifically compared with total finger blood flow, nor is it known how long it takes fingertip temperature to fully reflect an abrupt change in finger blood flow. Steady-state skin-temperature gradients were compared with total fingertip blood flow in 19 healthy volunteers. There was an excellent correlation between steady-state skin-surface temperature gradients and total fingertip blood flow measured with venous-occlusion volume plethysmography: gradient = 0.2-5.7.log(flow), r = 0.98. The half-time for fingertip cooling after complete arterial obstruction (in 8 volunteers) was 6.6 +/- 1.2 min. The authors conclude that skin-temperature gradients are an accurate measure of thermoregulatory peripheral vasoconstriction.
Until recently, the endothelium was regarded as a relatively inert cell layer. However, over the past 20 years, research has revealed an extraordinary array of endothelial functions, including control over coagulation, fibrinolysis, arterial tone and vascular growth. Importantly, endothelial dysfunction has been implicated as a key event in the pathogenesis of atherosclerosis, coronary vasoconstriction and, probably, myocardial ischemia. The recent demonstration that endothelial dysfunction may be reversible raises the possibility of slowing the progression of atherosclerosis or modifying arterial function, or both, to decrease the risk of acute cardiovascular events.
The purpose of this study was to test the hypothesis that cholesterol levels in the high normal range are associated with impaired endothelium-dependent vasodilation.
We studied leg blood flow (LBF) responses to graded intrafemoral artery infusions of the endothelium-dependent vasodilator methacholine chloride (MCh) or the endothelium-independent vasodilator sodium nitroprusside (SNP) in normal volunteers exhibiting a wide range of total cholesterol levels within the normal range (<75th percentile). LBF increased in a dose-dependent fashion in response to the femoral artery infusions of MCh and SNP (P<.001). LBF responses to MCh were significantly blunted (P<.001) in subjects with high normal cholesterol (195+/-6 mg/dL, n=13) compared with subjects with low normal cholesterol (146+/-5 mg/dL, n=20). Maximal endothelium-dependent vasodilation in the high normal group was decreased by nearly 50% compared with the low normal group (146+/-13% versus 268+/-34%, P<.01). There was a negative correlation between total cholesterol levels and maximal endothelium-dependent vasodilation (total cholesterol, r=-.41, P<.02; LDL cholesterol, r=-.42, P<.02). On the other hand, LBF responses to the endothelium-independent vasodilator SNP did not differ between groups.
These data suggest that an inverse and continuous relationship exists between the prevailing cholesterol level and endothelium-dependent vasodilation. Moreover, cholesterol levels even in the normal range may be associated with endothelial dysfunction, thus potentially contributing to the increased risk of macrovascular disease conferred by cholesterol elevations.
Patients with heart failure demonstrate attenuated endothelium-dependent vasodilation of the peripheral circulation, while this is suggested to be reversed after heart transplantation. However, data from human subjects are limited and conflict with studies on the peripheral vasomotor tone in cyclosporine-treated animals, suggesting endothelial dysfunction. We recorded forearm skin perfusion responses following graded iontophoresis of 1% acetylcholine (endothelium-dependent) and 1% sodium nitroprusside (endothelium-independent) by laser Doppler perfusion measurements in 32 heart transplant recipients and 15 age-matched controls. In addition, the hyperemic response to 3 min of blood flow occlusion to the forearm was measured on the third finger pulp. With comparable baseline values, the increases in perfusion to the 4 applications of acetylcholine were significantly attenuated in heart transplant recipients compared with controls: 59 +/- 9 vs. 146 +/- 32, 242 +/- 39 vs. 492 +/- 77, 480 +/- 66 vs. 845 +/- 120 and 699 +/- 77 vs. 993 +/- 139% (mean +/- SEM; all p < 0.01). Peak hyperemia (134 +/- 4 vs. 153 +/- 12 arbitrary units (AU); p < 0.05)), time for the hyperemic perfusion to return to preocclusive baseline (52.4 vs. 102.9 s; p < 0.01) and hence the area under the perfusion curve (1469 +/- 244 vs. 4581 +/- 921 AU s; p < 0.01) were reduced among heart transplant recipients. The area under the perfusion curve correlated significantly with mean arterial blood pressure (r = -0.60; p < 0.01) and with the responses to iontophoresis of acetylcholine (r = 0.41; p < 0.01). Two non-invasive tests of vascular function demonstrate attenuated endothelial-dependent microvascular responses in heart transplant recipients. The relative impact of prior congestive heart failure and postoperative factors, such as treatment with cyclosporine, remains to be determined.
The purpose of this study was to determine the effects of systemic exercise training on endothelium-mediated arteriolar vasodilation of the lower limb and its relation to exercise capacity in chronic heart failure (CHF). Endothelial dysfunction is a key feature of CHF, contributing to increased peripheral vasoconstriction and impaired exercise capacity. Local handgrip exercise has previously been shown to enhance endothelium-dependent vasodilation in conduit and resistance vessels in CHF.
Twenty patients were prospectively randomized to a training group (n=10, left ventricular ejection fraction [LVEF] 24+/-4%) or a control group (n=10, LVEF 23+/-3%). At baseline and after 6 months, peak flow velocity was measured in the left femoral artery using a Doppler wire; vessel diameter was determined by quantitative angiography. Peripheral blood flow was calculated from average peak velocity (APV) and arterial cross-sectional area. After exercise training, nitroglycerin-induced endothelium-independent vasodilation remained unaltered (271% versus 281%, P=NS). Peripheral blood flow improved significantly in response to 90 microg/min acetylcholine by 203% (from 152+/-79 to 461+/-104 mL/min, P<0.05 versus control group) and the inhibiting effect of L-NMMA increased by 174% (from -46+/-25 to -126+/-19 mL/min, P<0.05 versus control group). Peak oxygen uptake increased by 26% (P<0.01 versus control group). The increase in peak oxygen uptake was correlated with the endothelium-dependent change in peripheral blood flow (r=0.64, P<0. 005).
Regular physical exercise improves both basal endothelial nitric oxide (NO) formation and agonist-mediated endothelium-dependent vasodilation of the skeletal muscle vasculature in patients with CHF. The correction of endothelium dysfunction is associated with a significant increase in exercise capacity.
It has been postulated that lymphatic insufficiency may have a key role in pressure ulcer development. Our hypothesis is that the particular dynamic action of the Airwave mattress directly improves lymphatic circulation compared to conventional hospital mattresses.
Seven anesthetized sheep (40-48 kg) prepared with chronic prefemoral lymph fistulas and vascular catheters were first placed on a standard hospital mattress. Following 30 minutes of equilibration, a 2 hr control period was started measuring lymph flow and vascular pressures. The standard mattress was then exchanged for an active Airwave mattress (Pegasus Egerton, Ltd.) and after 30 minutes of equilibration monitored as above. After 2.5 hr, the support surface was then switched back to the standard mattress and monitored as before. Data are mean +/- sem.
Initially, on the standard mattress, lymph flow was 1.0 +/- 0.2 ml/30 min and increased significantly more than 3 fold on the Aireave mattress to 3.7 +/- 0.7 ml/30 min. Upon return to the standard mattress, lymph flow decreased to 1.2 +/- 0.2 ml/30 min. Hemodynamic variables and arterial blood gases were constant. Lymphatic protein transport increased significantly from 1.3 +/- 0.3 micrograms/min to 4.3 +/- 1.0 micrograms/min when placed on the test mattress and decreased when returned to the standard mattress to 1.3 +/- 0.2 micrograms/min. Similar rates of lymph flow were seen upon a variant of the Airwave mattress (Cairwave Therapy System).
Results support the hypothesis that the Airwave's action increased the lymph flow compared to a standard hospital mattress. The dynamic cycle may act to aid the pumping action of lymphatics by reducing pressure which would otherwise collapse and compress lymphatics leading to local edema and tissue swelling.
There are many reports of how IPC is used effectively in the clinical setting; including the prevention of deep venous thrombosis, improvement of circulation in patients with lower extremity arterial diseases, reduction of lymphoedema, and the healing of venous ulcers. However, despite the widely accepted use of IPC, it is still unclear how IPC actually exerts its beneficial effects. The exact physiological mechanisms of action are unknown. The clinical utility of IPC and the putative mechanisms by which IPC could exert its therapeutic effect will be reviewed. The paper will examine the mechanical effects of IPC exerted on the lower extremity, and the subsequent biochemical changes in the circulation. In vitro studies of the effects of mechanical stress such as compressive strain and shear on cultured endothelial cells, and their clinical relevance to IPC will also be reviewed.
A mathematical model of the cardiovascular system is simulated numerically. The basic unit in the model is an oscillator that possesses a structural stability and robustness motivated by physiological understanding and by the analysis of measured time series. Oscillators with linear couplings are found to reproduce the main characteristic features of the experimentally obtained spectra. To explain the variability of cardiac and respiratory frequencies, however, it is essential to take into account the rest of the system, i.e. to consider the effect of noise. It is found that the addition of noise also results in epochs of synchronization, as observed experimentally. Preliminary analysis suggests that there is a mixture of linear and parametric couplings, but that the linear coupling seems to dominate.
Postocclusive reactive hyperemia (PORH) was evaluated in three healthy volunteers and in three patients with different etiologies and suffering from peripheral arterial occlusive disease (PAOD). Three noninvasive methods were used: transcutaneous oximetry (TcPO2), near-infrared spectroscopy (NIRS), and laser Doppler flowmetry (LDF). Changes in perfusion and oxygenation of tissue were measured on foot before, during, and after arterial occlusion on thigh. Numerical parameters were derived from measured signals for quantification of the PORH response. Results of all three methods provided distinction between healthy volunteers and patients. The experimental optical techniques of NIRS and LDF demonstrated more clearly than the well-established TcPO2 method the difference between healthy volunteers and patients. The dynamics of the PORH response proved to be a better indicator of peripheral vascular disorder than the amplitude of responses.
There is an age related decline in various physiological processes. Vascular ageing is associated with changes in the mechanical and the structural properties of the vascular wall, which leads to the loss of arterial elasticity and reduced arterial compliance. Arterial compliance can be measured by different parameters like pulse wave velocity, augmentation index, and systemic arterial compliance. There is evidence that arterial compliance is reduced in disease states such as hypertension, diabetes, and end stage renal failure. Changes in arterial compliance can be present before the clinical manifestation of cardiovascular disease. Pharmacological and non-pharmacological measures have been shown to improve arterial compliance. Arterial compliance may constitute an early cardiovascular risk marker and may be useful in assessing the effects of drugs on the cardiovascular system. Pharmacogenetics and genetics of arterial compliance in the future will improve our knowledge and understanding about vascular ageing.
This study investigated the effects of aromatherapy massage on the lipid profile and blood pressure in Korean climacteric women. A wait-listed control group, pretest-posttest design was used. The subjects comprised 58 climacteric women: 30 in the experimental group and 28 in the control group. Aromatherapy massage using lavender, rose geranium, rose, and jasmine was given to the experimental group only. Each massage session lasted 30 minutes, and was performed once weekly for two 8-week periods with self abdominal daily massage at home. The intervention produced significant differences in the systolic blood pressure compare to pretreatment and significant differences in systolic and diastolic blood pressures at posttreatment between the two groups. These results suggest that aromatherapy massage may exert positive effects on blood pressure. However, more objective, clinical measures should be applied in a future study with a randomized placebo-controlled design.
Heels have substantially higher tissue interface pressures and are prone to ulceration compared to other bony prominences. Although many different types of alternating pressure air mattresses (APAMs) are used for the prevention and treatment of pressure ulcers, a few high-quality randomised controlled trials (RCTs) are available on which to base purchasing decisions. Faced with this situation, physiological measurements are increasingly being used as a surrogate. A time-based technique, which calculates pressure relief index (PRI), has been previously reported for analysing the ability of such systems. This technique has demonstrated that different designs produce variable results in this regard. The aim of the present study is to investigate the performance of three APAMs using PRI and blood perfusion measurements. Eleven able-bodied adult volunteers (6 males and 5 females) participated in the study. Their age, weight, height and body mass index (BMI) were (mean +/- s.d.) 23.9 +/- 2.1 years, 65.6 +/- 12.4 kg, 1.76 +/- 0.84 m and 21.0 +/- 2.4 kg/m2, respectively. There was no statistically significant difference in maximum interface pressure for the three mattresses. However, the AUTOlogic produced a statistically significant lower minimum interface pressure (Duo Care Plus, p < 0.0001 and higher pressure relief index below 30 mmHg than either the Duo Care Plus, p = 0.002 or Proficare, p < 0.0001. The AUTOlogic also gave a statistically significant enhanced perfusion per cycle when compared to other two mattresses (Duo Care Plus, p = 0.03 or Proficare, p = 0.01).
Metabolic and vascular abnormalities have been found in individuals with type 2 diabetes mellitus (T2D). Family history is often associated with increased risk of the development of T2D. We sought to determine if young, sedentary, insulin-sensitive individuals with a family history of T2D (FH+) have a reduced resting energy expenditure (REE) and vascular endothelial function compared with individuals who have no family history of T2D (FH-). The REE was determined in 18 FH+ individuals and 15 FH- individuals using indirect open-circuit calorimetry. Vascular endothelial function was measured via flow-mediated dilation (FMD) of the brachial artery. C-reactive protein and interleukin-6 were also measured to look at vascular inflammation. Body composition was measured via bioelectrical impedance analysis to determine fat-free mass and fat mass for each individual. Insulin resistance was calculated using the homeostasis model assessment equation and fasting insulin and glucose concentrations. Subjects (n = 42) were approximately 26 years old and had normal fasting serum insulin or glucose concentrations. The REE normalized for body weight (kilocalories per day per kilogram body weight) was significantly reduced in the FH+ women compared with FH- women (P < .001) but not in the men. The FMD was significantly reduced (34.3%) in the FH+ group compared with the FH- in women (P = .002). However, no between-group difference in FMD was present in male subjects (P = .376). Young, healthy, insulin-sensitive women with a family history of T2D have reduced whole-body metabolic rate and vascular endothelial function compared with those with no family history of disease. These differences in whole-body metabolic rate and vascular endothelial function were not present in male subjects.
- Posada-Moreno P
- Joly HR
Defining active pressure redistribution
- L Phillips
- R Goossens
- M Takahashi
- M Clark
Phillips L, Goossens R, Takahashi M, Clark M. Defining active pressure
redistribution. Wounds International. 2012; 3(1):52-56.
Effect of Intermittent Pneumatic Compression Therapy on Healing of Diabetic Foot Ulcer
- F Mohamed
- H El-Deen
Mohamed F, El-deen H. Effect of Intermittent Pneumatic Compression
Therapy on Healing of Diabetic Foot Ulcer. International Journal of
Diabetes Research 2015; 4(4):67-72
An intermittent pneumatic
- E Hanson
- K Stetter
- R Li
- A Thomas
Hanson E, Stetter K, Li R, Thomas A. An intermittent pneumatic
Temperature of the great toe as an indication of the severity of shock
- H R Joly
- M H Weil
Joly HR, Weil MH. Temperature of the great toe as an indication of
the severity of shock. Circulation 1969; 39(1):131-138. https://doi.
org/10.1161/01.CIR.39.1.131
Influence of different bed support surface covers on skin temperature
- P Posada-Moreno
- Elena Losa Iglesias
- Becerro De Bengoa
- R Vallejo
Posada-Moreno P, Elena Losa Iglesias M, Becerro De Bengoa Vallejo
R et al. Influence of different bed support surface covers on skin
temperature. Contemp Nurse 2011; 39(2):206-220. https://doi.
org/10.5172/conu.2011.39.2.206