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Canadian Journal of Anaesthesia 04/2012; 54:44598-44598. · 2.35 Impact Factor
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ABSTRACT: To evaluate the efficacy and safety of dexmedetomidine for emergence agitation after tonsillectomy in children.
120 ASA physical status I and II children, aged 5-14 years, undergoing anesthesia for tonsillectomy, were randomly divided into 3 groups: Placebo group, the low dexmedetomidine concentration group and the high dexmedetomidine concentration group. Before the entrance of the operating room (OR), all of the children received intravenous injection 40 μg kg(-1) midazolam to reduce anxiety at first, and then dexmedetomidine was given intravenously at an initial loading dose of 0.5 μg kg(-1) or 1 μg/kg over a 10-min period via a computer controlled infusion pump followed by a maintenance infusion of 0.2 μg kg(-1)h(-1) or 0.4 μg kg(-1)h(-1)over the surgery. The heart rate, SpO(2) and mean arterial blood pressure were recorded for each patient in both operation room and PACU. The designated time points: at the start of the anesthetic induction, at the discontinuation of inhalational agents, at first opening of eyes, at time to remove endotracheal tube were recorded. After patient arrival at the PACU, VAS score, RSS, the occurrence of emergence agitation were recorded every 5 min for the first 30 min and every 10 min for the next 30 min after endotracheal tube was removed.
There was significant difference in the incidence of emergence agitation between Placebo group and the high concentration group when endotracheal tube was removed (P<0.05). There was significant difference in the VAS pain scores and in the RSS between three groups at the time of extubation, as well as 5 min and 10 min after extubation (P<0.05).
Dexmedetomidine appears to be safe and effective to reduce the incidence of early emergence agitation in children after tonsillectomy. Initial loading dose of 1.0 μg kg(-1) followed by a maintenance infusion of 0.4 μg kg(-1)h(-1) is better choice for children received tonsillectomy.
International journal of pediatric otorhinolaryngology 04/2012; 76(7):1036-41. · 0.85 Impact Factor
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ABSTRACT: To investigate the effects of ligustrazine on acute lung injury induced by blunt chest trauma.
This study was performed in the Animal Center of Renmin Hospital of Wuhan University, Wuhan, China between September 2009 and September 2010. Male Sprague-Dawley rats were randomly allocated into 4 groups: sham control group (group C, n=60), ligustrazine treatment group (group C+L, n=60), blunt chest trauma model group (group T, n=60), and the trauma plus ligustrazine treatment group (group T+L, n=60). The lung contusion was induced as previously described. Animals of the T+L group were intraperitoneally injected with ligustrazine. Acute lung injury was evaluated by histopathology of the lung, and apoptosis was determined by terminal dUTP nick-labeling. Pulmonary edema was estimated using Evans blue dye extravasation and wet/dry ratios of lung tissue. The expression of caspase-3, Bcl-2, and Bax in the lung, as well as blood plasma tumor necrosis factor (TNF)-alpha were also measured.
The ligustrazine treatment significantly attenuated lung injury induced by blunt chest trauma, as shown by decreased apoptosis index, and pulmonary edema (p=0.04). The blood plasma TNF-alpha level after blunt chest trauma significantly deceased after the administration of ligustrazine (p=0.03). In addition, the ligustrazine treatment significantly alleviated the expression of caspase-3 (p=0.03), and increased the ratio of Bcl-2 to Bax (p<0.03).
Ligustrazine effectively protects lung injury induced by blunt chest trauma, and the protective effects seem to be mediated by attenuation of cell apoptosis via an increased ratio of Bcl-2/Bax and decreased caspase-3 activity.
Saudi medical journal 02/2012; 33(2):139-45. · 0.52 Impact Factor
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ABSTRACT: Toll-like receptor 4 (TLR4) is widely recognised as a pattern recognition receptor (PRR) in the triggering of innate immunity. Lung inflammation and systemic innate immune responses are dependent on TLR4 activation undergoing pulmonary contusion. Therefore, the author investigated the effects of penehyclidine hydrochloride (PHC) on the expression of TLR4 and inflammatory responses of blunt chest trauma-induced pulmonary contusion.
Male Sprague-Dawley (SD) rats were randomly assigned into three groups: normal control (NC) group, pulmonary contusion (PC) group and penehyclidine hydrochloride treatment (PHC) group. Pulmonary contusion was induced in anesthetised rats at fixed chest impact energy of 2.45J. Lung injury was assessed by the histopathology changes, arterial blood gas and myeloperoxidase (MPO) activity of lung. The serum tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels were measured using enzyme-linked immunosorbent assays (ELISA). The expression of TLR4 was determined by immunohistochemistry.
Blunt chest trauma produced leucocytosis in the interstitial capillaries, hypoxemia, and increased MPO activity. The expressions of TNF-α, IL-6 and TLR4 in the lung were significantly enhanced during pulmonary contusion. PHC treatments effectively attenuated pulmonary inflammation responses, as shown by improved pulmonary oxygenation, histopathology damage, decreased the MPO activity, the expressions of TNF-α, IL-6, and TLR4 after lung injury.
It might be concluded that PHC exhibit anti-inflammatory and protective effects in traumatic lung injury via the inhibition of the TLR4 pathway.
Injury 11/2011; 43(2):232-6. · 1.98 Impact Factor
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ABSTRACT: Phosphocreatine (PCr) is an endogenous compound containing high-energy phosphate bonds. It has been confirmed that PCr is effective in preventing and treating cardiac and renal ischemia-reperfusion injury. In this study, rat cerebral ischemia-reperfusion injury models were constructed. Apoptotic cells in the cortex region were measured by TUNEL method. Malondialdehyde (MDA) content was detected by chromatometry, and calmodulin (CaM) activity was detected by ELISA. Compared with sham-operated group (sham group), TUNEL-positive cells, MDA, and level of CaM activity increased in ischemia-reperfusion group (I/R group) and PCr preconditioning group (PCr group); compared with I/R group, TUNEL-positive cells, MDA content, and level of CaM activity decreased in PCr group. This study indicated that PCr can decrease the morphological damage and the neuron apoptosis of the ischemia-reperfusion injury brain through attenuating abnormalities of calcium balance and production of oxygen free radicals.
Journal of Biomedicine and Biotechnology 01/2011; 2011:107091. · 2.44 Impact Factor
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ABSTRACT: Vascular endothelial growth factor (VEGF) plays important roles in establishing collateral circulation of ischemic myocardium. This study aimed to investigate the effect of isoflurane on VEGF expression and the potential intracellular signal transduction pathway in cultured rat myocardial cells in order to further reveal the molecular mechanism of myocardial preservation of isoflurane.
Primary myocardial cells of Sprague-Dawley rats were isolated and cultured. They were divided randomly into control group, isoflurane group, protein kinase C (PKC) inhibitor group and PKC inhibitor+isoflurane group where cells were respectively incubated without any treatment, treated by 0.5, 1.0 and 1.5 minimum alveolar concentration (MAC) of isoflurane for 6 hours, by PKC inhibitor calphostin C at a final concentration of 50 nmol/L and by 50 nmol/L calphostin C+1.0 MAC isoflurane for 6 hours. VEGF expression was detected by enzyme-linked immunosorbent assay (ELISA) and the expression levels of PKC isoforms were determined by Western immunoblotting method.
Isoflurane increased the VEGF expression in myocardial cells in a dose-dependent way. VEGF levels were significantly higher in 1.0 and 1.5 MAC isoflurane groups than in the control group (both P < 0.01). The effect of isoflurane on upregulating VEGF expression was blocked by PKC inhibitor calphostin C (P < 0.01), but calphostin C did not alter VEGF expression (P > 0.05). Isoflurane induced the activation and translocation of PKCε. Immunoblotting analysis revealed that the immunoreactivity of PKC ε increased significantly in the membrane fractions and deceased significantly in the kytoplasm fractions for cells treated with 1.0 MAC isoflurane as compared with the untreated cells, but not of PKC-α, PKC-δ and PKC-ζ (P less than 0.01).
Isoflurane induces myocardial cells to release VEGF through activating PKC-epsilon from the endochylema to the cytomembrane, suggesting a possible novel mechanism of isoflurane protecting myocardial cells.
Chinese Journal of Traumatology (English Edition) 10/2010; 13(5):284-8.
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ABSTRACT: Supplementation of L-arginine, a nitric oxide precursor, during the late phase of myocardial ischemia/reperfusion increases myocyte apoptosis and exacerbates myocardial injury, but the underlying mechanism is unclear. During myocardial ischemia/reperfusion, apoptosis of endothelial cells precedes that of cardiomyocyte. Tumor necrosis factor-alpha (TNF) production is increased during myocardial ischemia/reperfusion, which may exacerbate myocardial injury by inducing endothelial cell apoptosis. We postulated that L-arginine may exacerbate TNF-induced endothelial cell apoptosis by enhancing peroxynitrite-mediated nitrative stress. Cultured human umbilical vein endothelial cells were either not treated (control) or treated with TNF alone or with TNF in the presence of L-arginine, the nonselective nitric oxide synthase inhibitor N (omega)-nitro-L-arginine (L-NNA), propofol (an anesthetic that scavenges peroxynitrite), or L-arginine plus propofol, respectively, for 24 hours. TNF increased intracellular superoxide and hydrogen peroxide production accompanied by increases of inducible nitric oxide synthase (iNOS) protein expression and nitric oxide production. This was accompanied by increased protein expression of nitrotyrosine, a fingerprint of peroxynitrite and an index of nitrative stress, and increased endothelial cell apoptosis. L-arginine did not enhance TNF-induced increases of superoxide and peroxynitrite production but further increased TNF-induced increase of nitrotyrosine production and exacerbated TNF-mediated cell apoptosis. L-NNA and propofol, respectively, reduced TNF-induced nitrative stress and attenuated TNF cellular toxicity. The L-arginine-mediated enhancement of nitrative stress and TNF toxicity was attenuated by propofol. Thus, under pathological conditions associated with increased TNF production, L-arginine supplementation may further exacerbate TNF cellular toxicity by enhancing nitrative stress.
Journal of cardiovascular pharmacology 04/2010; 55(4):358-67. · 2.83 Impact Factor
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ABSTRACT: Propofol concentrations that produce laboratory-based cardioprotective effects are generally greater than those produced under routine anesthesia during cardiac surgery. It is unknown whether experimental cardioprotective propofol concentrations can routinely be achieved during cardiopulmonary bypass (CPB) using continuous infusion.
Twenty-four patients scheduled for primary aortocoronary bypass grafting with CPB were allocated to receive one of three propofol infusion rates; 50, 100, or 150 microg x kg(-1) x min(-1) in an open-label pilot study. Data were described using a line of best fit to derive an experimental clinical maneuver predicted to produce a whole blood concentration of 5 microg x mL(-1) at reperfusion. A predetermined interim analysis of 30 patients who were receiving the derived maneuver in an ongoing study was used to evaluate the maneuver. Cardiac index (CI), systemic vascular resistance index (SVRI), and left ventricular stroke work index (LVSWI) were recorded.
The infusion rate-concentration curve had an equation of y = 0.215e (0.0279x ), where y represents the whole blood concentration and x represents the infusion rate (r (2) = 0.781). The predicted infusion rate to achieve a mean concentration of 5 microg x mL(-1) was 113 microg x kg(-1) x min(-1). The nearest practical rate is 120 microg x kg(-1) x min(-1), producing a concentration of 5.39 (1.45) microg x mL(-1). The values for CI, SVRI, and LVSWI were similar between groups at corresponding time periods.
An infusion rate of 120 microg x kg(-1) x min(-1) is clinically practical and capable of achieving experimental cardioprotective propofol concentrations at reperfusion.
Canadian Anaesthetists? Society Journal 08/2009; 56(9):658-66. · 2.31 Impact Factor
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ABSTRACT: The emergence of ischaemic post-conditioning (IPO) provides a potential method for experimentally and clinically attenuating various types of organ injuries. There has been little work, however, examining its effects in the setting of lung ischaemia reperfusion (IR). The stress protein, haeme oxygenase-1 (HO-1), has been found to exert a potent, protective role in a variety of lung injury models. In this study, we hypothesised that the induction of HO-1 by IPO plays a protective role against the deleterious effects of IR in the lung.
Anaesthetised and mechanically ventilated adult Sprague-Dawley rats were randomly assigned to one of the following groups (n=8 each): the sham-operated control group, the IR group (40 min of left-lung ischaemia and 105 min of reperfusion), the IPO group (three successive cycles of 30-s reperfusion per 30-s occlusion before restoring full perfusion) and the ZnPPIX+IPO group (ZnPPIX, an inhibitor of HO-1, was injected intra-peritoneally at 20 mg kg(-1) 24h prior to the experiment and the rest of the procedures were similar to that of the IPO group). Lung injury was assessed by arterial blood gas analysis, wet-to-dry lung weight ratio and tissue histological changes. The extent of lipid peroxidation was determined by measuring plasma levels of malondialdehyde (MDA) production. Expression of HO-1 was determined by immunohistochemistry.
Lung IR resulted in a significant reduction of PaO(2) (data in IR, P<0.05 vs. data in sham) and increase of lung wet-to-dry weight ratio, accompanied with increased MDA production and severe lung pathological morphological changes as well as a compensatory increase in HO-1 protein expression, as compared with sham (All P<0.05). IPO markedly attenuated all the above pathological changes seen in the IR group and further increased HO-1 expression. Treatment with ZnPPIX abolished all the protective effects of post-conditioning.
It may be concluded that IPO protects IR-induced lung injury via induction of HO-1.
Injury 07/2009; 41(5):510-6. · 1.98 Impact Factor
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ABSTRACT: Vascular endothelial cells play an important role in maintaining cardiovascular homeostasis. Oxidative stress is a critical pathogenic factor in endothelial cell damage and the development of cardiovascular diseases. In this study we evaluated the effects of propofol on oxidative stress-induced endothelial cell insults and the role of serine-threonine kinase Akt modulation of endothelial nitric oxide synthase (eNOS) as a mechanism of protection.
Human umbilical vein endothelial cells were used as the experimental model. Hydrogen peroxide (H2O2, 100 microM) was used as the stimulus of oxidative stress. Study groups included 1) control; 2) cells incubated with H2O2 alone; 3) cells incubated with propofol (50 microM) alone; or 4) cells pretreated with propofol 50 microM for 30 min then co-incubated with H2O2. Cell viability was assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and Trypan blue dye exclusion test. Cell apoptosis was evaluated by Hoechst 33258 staining. Caspase-3 activity was determined by the colorimetric CaspACE Assay System. Expressions of Akt, phospho-Akt, and eNOS were detected by Western blotting.
H2O2 decreased cell viability, induced apoptosis, and increased caspase-3 activity in human umbilical vein endothelial cells. Propofol significantly protected cells from H2O2-induced cell damage, apoptosis and decreased H2O2-induced increase in caspase-3 activity. Propofol treatment significantly increased eNOS expression compared to control and H2O2-stimulated cells. There was no significant difference in phospho-Akt (Ser 473 or Thr 308) expression among the groups.
Propofol 50 microM can reduce H2O2-induced damage and apoptosis in endothelial cells, by suppressing caspase-3 activity and by increasing eNOS expression via an Akt-independent mechanism.
Anesthesia and analgesia 11/2007; 105(4):1027-33, table of contents. · 3.08 Impact Factor
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ABSTRACT: The circulatory inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) is increased in pathological conditions, such as diabetes, which initiate or exacerbate vascular endothelial injury. Both nitric oxide (NO) and reactive oxygen species may play a dual role (i.e., inhibiting or promoting) in TNF-alpha-induced endothelial cell apoptosis. We investigated the effects of the antioxidant N-acetylcysteine on TNF-alpha-induced apoptosis in human vascular endothelial cell (cell line ECV304) apoptosis, NO production and lipid peroxidation. Cultured vascular endothelial cell (ECV304) were either not treated (control), or treated with TNF-alpha (40 ng/ml) alone or TNF-alpha in the presence of N-acetylcysteine at 30 mmol/l or 1 mmol/l, respectively, for 24 h. Cell viability was measured by MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay. Cell apoptosis was assessed by flow cytometry. TNF-alpha-induced endothelial cell apoptosis was associated with increased inducible NO synthase but reduced endothelial NO synthase (eNOS) protein expression. NO production and the levels of the lipid peroxidation product malondialdehyde were concomitantly increased. Treatment with NAC at 30 mmol/l restored eNOS expression and further increased NO production as compared to TNF-alpha alone, resulting in improved cell viability and reduced apoptosis. This was accompanied by increased superoxide dismutase activity, increased glutathione peroxidase production and reduced malondialdehyde levels. N-acetylcysteine at 1 mmol/l, however, did not have significant effects on TNF-alpha-induced endothelial cell apoptosis and cell viability despite it slightly enhanced glutathione peroxidase production. N-acetylcysteine attenuation of TNF-alpha-induced human vascular endothelial cell apoptosis is associated with the restoration of eNOS expression.
European Journal of Pharmacology 12/2006; 550(1-3):134-42. · 2.52 Impact Factor
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ABSTRACT: We designed the present study to test the hypothesis that oxygen free radicals can enhance tumor necrosis factor (TNF)-alpha cellular toxicity, which might be reversed by propofol, an anesthetic with antioxidant properties, in human vascular endothelial cell line ECV304. Cultured ECV304 were either not treated, treated with 10 muM of hydrogen peroxide (H2O2), treated with TNF-alpha (40 ng/mL) alone, TNF-alpha in the presence of 10 microM of H2O2 (H+T), or propofol plus H2O2 for 24 h. Cell viability was measured by lactate dehydrogenate (LDH) assay. Cell apoptosis was assessed by flow cytometry and terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP) nick end-labeling. The antiapoptotic Bcl-2 and pro-apoptotic Bax protein expressions were measured by immunocytochemical analysis. Increases in apoptosis, Bax, lipid peroxidation product malondialdehyde, LDH, and decreases in Bcl-2, superoxide dismutase, and glutathione peroxidase were observed in TNF-alpha-treated cells. H2O2 10 microM did not cause significant lipid peroxidation (0.75 +/- 0.03 nmol/mg of malondialdehyde protein) as compared with control (0.70 +/- 0.04 nmol/mg of malondialdehyde protein) (P > 0.05) but further enhanced TNF-alpha-induced lipid peroxidation, upregulated Bax, and down-regulated Bcl-2 expression and enhanced TNF-alpha-induced cell apoptosis (P < 0.05). Propofol 50 microM attenuated TNF-alpha and H2O2-induced cell apoptosis, accompanied by decreases in malondialdehyde and LDH production and restoration of Bcl-2 expression. Propofol exerts protective effects against H2O2-enhanced TNF-alpha cell toxicity by reducing oxidative injury.
Anesthesia and analgesia 08/2006; 103(1):110-6, table of contents. · 3.08 Impact Factor
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Anesthesiology 03/2006; 104(2):383-4; author reply 384-5. · 5.36 Impact Factor
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Chinese medical journal 09/2005; 118(16):1388-91. · 0.86 Impact Factor
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ABSTRACT: This study was undertaken to demonstrate that gastrointestinal mucosal injury occurs during cardiopulmonary bypass in children, increasing systemic inflammatory responses, and to determine whether shen-fu injection (the major components of which are ginsenosides compound, extract of Panax ginseng shown to have antioxidant properties) could attenuate gastrointestinal mucosal injury and subsequent inflammatory responses.
Twenty-four children undergoing heart surgery for congenital heart defects were randomly assigned to groups C (placebo control, n = 12) and G (1.35 mg/kg ginsenosides compound intravenously before and throughout the course of cardiopulmonary bypass, n = 12). Central venous blood samples were taken before cardiopulmonary bypass and at 60 and 120 minutes after aortic declamping (reperfusion). Gastric intramucosal pH was measured by perioperative tonometry. Plasma lipid peroxidation product malondialdehyde, myocardium-specific creatine kinase isoenzyme MB activity, diamine oxidase, lipopolysaccharide, and interleukin 6 were all measured.
Significant decrease in gastric intramucosal pH and increase in plasma diamine oxidase were seen during reperfusion in group C, accompanied by increases in plasma levels of malondialdehyde, lipopolysaccharide, interleukin 6, and creatine kinase isoenzyme MB (P < .01 vs before cardiopulmonary bypass). Shen-fu injection significantly attenuated these changes (P < .05). Consequently, fewer patients in group G (2/12) than in group C (7/12) needed postoperative inotropic support. Postoperative intensive care unit stay was shorter in group G than in group C. A tight positive correlation was seen between diamine oxidase and interleukin 6 at 60 minutes after aortic declamping and between diamine oxidase and lipopolysaccharide at 120 minutes after aortic declamping (r = 0.79, P < .0001).
Ginsenosides compound may attenuate gastrointestinal injury and inhibit inflammatory response after cardiopulmonary bypass in patients with congenital heart disease.
Journal of Thoracic and Cardiovascular Surgery 09/2005; 130(2):258-64. · 3.41 Impact Factor
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ABSTRACT: We investigated whether propofol can inhibit tumor necrosis factor (TNF)-alpha-induced apoptosis in cultured human umbilical vein endothelial cells (HUVECs). Isolated HUVECs were cultured in Dulbecco's modified Eagle medium supplemented with 20% bovine calf serum. HUVECs in untreated and propofol control groups were cultured at 37 degrees C for 24.5 h. HUVECs in the TNF treatment groups were initially cultured for 30 min in the presence of TNF or various concentrations of propofol, respectively, which were then cultured for 24 h with the addition of TNF at 40 ng/mL in the medium. Apoptosis was detected using terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) and confirmed by electron microscopy. The antiapoptotic Bcl-2 and proapoptotic Bax protein expressions were measured by immunocytochemical analysis. TNF stimulation resulted in a reduced Bcl-2/Bax ratio and increased apoptotic index (AI: percentage of apoptotic cells) in HUVECs. Propofol, at concentrations >/=12 muM, significantly (P < 0.001) and dose-dependently attenuated TNF-induced increase in AI and decrease in Bcl-2/Bax ratio. This was accompanied by increases in nitric oxide production. There is an inverse correlation between the ratio of Bcl-2/Bax expression and AI (P = 0.0009). These results suggest that propofol, at clinical relevant concentrations, can reduce TNF-induced HUVEC apoptosis.
Anesthesia & Analgesia 07/2005; 100(6):1653-9. · 3.29 Impact Factor
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ABSTRACT: To identify the protective effects of hypovolemic hypotension preconditioning on cardiopulmonary function after myocardial ischemia/reperfusion injury and to explore the possible mechanism.
Twenty-four male white rabbits were randomly assigned to two groups. In the control group, ischemia/reperfusion animals(Group I/R, n=10) were subjected to thirty-minute occlusion of left anterior descending coronary artery and two-hour reperfusion. Animals in hypovolemic hypotension preconditioning group (Group HHP, n=14) experienced brief systemic ischemia preconditioning through blood withdrawal to lower blood pressure to 40%-50% of the baseline before myocardial ischemia/reperfusion. Hemodynamic parameters were recorded. Blood sample was taken to measure superoxide dismutase (SOD), malondialdehyde (MDA) and nitrogen monoxide (NO) changes with blood gas analysis. Myocardium specimens were sampled to examine apoptosis-related gene interleukin-1 beta converting enzyme (ICE) mRNA.
Cardiac mechanical function and lung gas exchange remained stable in Group HHP with a significant increase in NO level; while in Group I/R without preconditioning, cardiopulmonary dysfunction was present after 2 h reperfusion associated with a significant reduction in NO formation and an increase in MDA (P<0.001). There was negative expression of ICE mRNA in the two groups.
Hypovolemic hypotension preconditioning significantly improves cardiopulmonary function and increases NO formation and the protective benefit associated with hypovolemic hypotension preconditioning of the heart may be regulated through NO mediated mechanism.
Chinese Journal of Traumatology (English Edition) 12/2004; 7(6):368-71.
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ABSTRACT: We investigated whether transient systemic ischemia can precondition the heart against the ensuing ischemic insult. Rabbits were randomly divided into systemic ischemic preconditioning (SIP), hemodilution (HD) and control (C) groups. SIP was induced by rapidly withdrawing blood from femoral artery and maintaining the mean artery pressure at 50 mmHg for 10 min. Afterwards, 50% of the withdrawn blood was re-infused with equal volumes of 6% deferoxamine-conjugated hydroxyethyl-starch (D-HES). Hemodilution in HD group was achieved by withdrawing blood at 8 ml/kg accompanied by concomitant infusion of equal volumes of D-HES. Animals were subjected to 30 min of coronary artery occlusion followed by 120 min of reperfusion. Cardiac output (CO) (thermodilution method), plasma malondialdehyde and nitric oxide content were measured at baseline and until 120 (R120) min of reperfusion. At R120, CO in group-C was significantly lower than its baseline value, accompanied by a significant reduction in nitric oxide production and increase in malondialdehyde concentration; CO in group-SIP and group-HD maintained at baseline levels throughout reperfusion. At R120, CO in group-SIP, but not in group-HD, was significantly higher than that in group-C. It is concluded that transient SIP followed by hemodilution with D-HES facilitates early functional recovery of the ischemic-reperfused rabbit hearts.
Interactive cardiovascular and thoracic surgery 10/2004; 3(3):528-32.
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Anesthesiology 05/2004; 100(4):1038-9; author reply 1039-40. · 5.36 Impact Factor
