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ABSTRACT: In this study, we aimed to compare the effects of low- and high-quality cardiopulmonary resuscitation (CPR) on cardioprotection by induced hypothermia (IH) at 34[degrees]C and examine whether extracellular signal-regulated kinase or endothelial nitric oxide synthase mediates this cardioprotection. Left ventricle infarct sizes were evaluated in six groups of rat hearts (n = 6) following Langendorff perfusion and triphenyltetrazolium chloride staining. Controls underwent 30 min of global ischemia at 37[degrees]C, followed by 10 min of simulated low- or high-quality CPR reperfusion and 90 min of reperfusion at 75 mmHg. The IH groups underwent IH at 34[degrees]C during reperfusion. The U0126 group received U0126 (60 [mu]M)-an extracellular signal-regulated kinase inhibitor-during reperfusion at 34[degrees]C. The L-NIO (N5-(1-iminoethyl)-L-ornithine dihydrochloride) group received L-NIO (2 [mu]M)-an endothelial nitric oxide synthase inhibitor-5 min before global ischemia at 37[degrees]C to the end of reperfusion at 34[degrees]C. Infarct size did not significantly differ between the control and IH groups receiving low-quality CPR. However, IH with high-quality CPR reduced the infarct size from 47.2% +/- 10.2% to 26.0% +/- 9.4% (P = 0.005). U0126 reversed the IH-induced cardioprotection (45.9% +/- 9.4%, P = 0.010), whereas L-NIO had no significant effect. Cardiopulmonary resuscitation quality affects IH-induced cardioprotection. Extracellular signal-regulated kinase may mediate IH-induced cardioprotection.
Shock 01/2013; 39(6):527-532. · 2.85 Impact Factor
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ABSTRACT: Therapeutic hypothermia (TH) is widely used as a cardioprotective treatment for cardiac arrest. TH at 30-32°C during ischaemia and reperfusion has a cardioprotective effect. The aims of the study were to examine whether TH at 34°C with late induction (immediately after the start of reperfusion) has a cardioprotective effect and to determine if this effect is mediated by nitric oxide (NO) and phosphatidylinositol 3'-kinase (PI3K).
Langendorff perfusion of Sprague-Dawley rat hearts was initiated at 75 mmHg at 37°C. Left ventricle infarct sizes were evaluated by triphenyltetrazolium chloride staining after Langendorff perfusion in 6 groups (each n=7): control group; ischaemia group, with 34°C TH during ischaemia for 30 min and reperfusion for 180 min; reperfusion group, with 34°C TH induced solely during the reperfusion period; the l-NAME (NO synthase inhibitor), LY294002, and wortmannin (PI3K inhibitors) groups, which were treated similarly to the reperfusion group with the addition of each compound.
TH reduced the left ventricle infarct size from 54.2 ± 14.8% of the control group to 11.9 ± 6.3% (ischaemia group, p<0.001) and to 23.5 ± 10.5% (reperfusion group, p<0.001). l-NAME, LY294002, and wortmannin reversed the cardioprotective effect of TH induced during reperfusion to 42.5 ± 10.6% (p=0.009), 40.9 ± 4.1% (p=0.021), and 51.9±13.0% (p<0.001), respectively. Circulatory temperatures reached 34°C within 5 min in all groups subjected to TH.
TH of 34°C showed a cardioprotective effect even with late initiation of cooling during reperfusion. The effect was mediated by NO and PI3K.
Resuscitation 08/2011; 83(2):238-42. · 3.60 Impact Factor
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ABSTRACT: Dexmedetomidine is a highly selective α-2 adrenergic agonist used perioperatively. Dexmedetomidine's cardioprotective effect after myocardial ischaemia remains unknown. In this study, we administered dexmedetomidine after ischaemia to investigate its ability to protect the cardiac muscle from ischaemia-reperfusion injury in isolated rat hearts.
After a 30-min stop of perfusion, isolated rat hearts underwent reperfusion for 120 min. At the initiation of reperfusion, dexmedetomidine was administered for 25 min at concentrations of 0 nM (control group), 1 nM (Dex 1 group), and 10 nM (Dex 10 group). Yohimbine (an α-2 adrenergic antagonist) was administered in the manner as above in another group of isolated rat hearts at a concentration of 1 μM without dexmedetomidine (Yoh group) and at 1 μM with 10 nM dexmedetomidine (Yoh+Dex 10 group). The area of infarction was measured using 2,3,5-triphenyltetrazolium staining.
Dexmedetomidine administration did not influence haemodynamics or the coronary flow (CF), but did increase the myocardial infarct size. Neither concentration of dexmedetomidine affected the infarct size as the Dex 1 and Dex 10 groups had almost the same infarct size. The infarct size was 40.5±2.9% in the control group, 60.9±5.3% in the Dex 1 group, and 60.9±2.8% in the Dex 10 group. The infarct size was reduced in the yohimbine groups. The infarct size was 39.2±3.3% in the Yoh+Dex 10 group and 45.0±3.2% in the Yoh group.
Dexmedetomidine administration does not influence haemodynamics or CF, but does increase the cardiac infarct size. α-2 Adrenergic stimulation may induce this mechanism.
Resuscitation 12/2010; 81(12):1714-7. · 3.60 Impact Factor
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ABSTRACT: To observe the effect of age on the changes in heart rate variability (HRV) of adult amateur athletes after playing a soccer game, 20 male were divided into two groups: middle-aged (n = 10, 35-55 years) and aged (n = 10, 56-75 years). Before and after 2-hour soccer games, HRV and blood pressure were recorded. In both groups heart rate increased greatly after exercise (73.1 ± 14.8 bpm vs 102.6 ± 16.2 bpm, p < 0.01 and 71.1 ± 8.6 bpm vs 89.9 ± 15.5 bpm, p < 0.01). In the middle-aged group, systolic blood pressure (SBP) did not change (124.0 ± 12.0 mmHg vs 118.9 ± 11.7 mmHg), while the mean standard deviation of the N-N intervals (SDNN), square root of the mean squared differences of successive N-N intervals (RMSSD), total power (TP), low frequency (LF) power, and high frequency (HF) power changed significantly (p < 0.05); in the aged group SBP decreased from 147.2 ± 23.7 mmHg to 127.7 ± 24.7 mmHg (p < 0.01), but SDNN, RMSSD, TP, LF, and HF did not change. It seems that in aged people the accommodation capability of the autonomic nervous system is different from that in middle-aged people.
Research in Sports Medicine An International Journal 10/2010; 18(4):263-9.
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ABSTRACT: To determine the effect of landiolol on ischemic preconditioned rat hearts.
Isolated perfused rat hearts were divided into 8 groups. In the control group, there was no treatment before the 30-min global ischemia. In the landiolol infused groups, landiolol (100, 300, and 500 microM) was infused without ischemic preconditioning (IPC). In other groups, hearts were pretreated with 2 episodes of 5-min global ischemia and reperfusion before the 30-min ischemia. During the preconditioning, landiolol (0, 100, 300, and 500 microM) was infused.
Recoveries of coronary flow (CF) and myocardial oxygen consumption (MVO(2)) at the 120th min after global ischemia to 86 +/- 18 and 112 +/- 19% of the baseline in the IPC group was, respectively, significantly greater than that to 65 +/- 10 and 72 +/- 10% in the control group. Landiolol 300 microM also increased the CF and MVO(2) significantly (97 +/- 19 and 98 +/- 39%) compared to the control. IPC + landiolol 500 microM reduced the increase in LV end-diastolic pressure significantly compared to the control. IPC, landiolol (100, 300, and 500 microM), and IPC + landiolol (100, 300, and 500 microM) all decreased infarct sizes significantly to 23.5 +/- 15.2, 29.8 +/- 12.1, 30.2 +/- 13.3, 22.8 +/- 14.8, 21.6 +/- 7.8, 34.2 +/- 14.7 and 25.5 +/- 11.3% of the total left ventricular mass, respectively, compared to the control (53.3 +/- 12.5%), but there were no significant differences among these groups.
IPC and landiolol have cardioprotective effects on ischemia-reperfusion injury in isolated rat hearts, but pretreatment with landiolol does not enhance the cardioprotective effect of IPC.
Journal of Anesthesia 04/2010; 24(2):208-14. · 0.83 Impact Factor
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ABSTRACT: Advancing a tracheal tube into the bronchus produces unilateral breath sounds. We created a Visual Stethoscope that allows real-time fast Fourier transformation of the sound signal and 3-dimensional (frequency-amplitude-time) color rendering of the results on a personal computer with simultaneous processing of 2 individual sound signals. The aim of this study was to evaluate whether the Visual Stethoscope can detect bronchial intubation in comparison with auscultation.
After induction of general anesthesia, the trachea was intubated with a tracheal tube. The distance from the incisors to the carina was measured using a fiberoptic bronchoscope. While the anesthesiologist advanced the tracheal tube from the trachea to the bronchus, another anesthesiologist auscultated breath sounds to detect changes of the breath sounds and/or disappearance of bilateral breath sounds for every 1 cm that the tracheal tube was advanced. Two precordial stethoscopes placed at the left and right sides of the chest were used to record breath sounds simultaneously. Subsequently, at a later date, we randomly entered the recorded breath sounds into the Visual Stethoscope. The same anesthesiologist observed the visualized breath sounds on the personal computer screen processed by the Visual Stethoscope to examine changes of breath sounds and/or disappearance of bilateral breath sound. We compared the decision made based on auscultation with that made based on the results of the visualized breath sounds using the Visual Stethoscope.
Thirty patients were enrolled in the study. When irregular breath sounds were auscultated, the tip of the tracheal tube was located at 0.6 +/- 1.2 cm on the bronchial side of the carina. Using the Visual Stethoscope, when there were any changes of the shape of the visualized breath sound, the tube was located at 0.4 +/- 0.8 cm on the tracheal side of the carina (P < 0.01). When unilateral breath sounds were auscultated, the tube was located at 2.6 +/- 1.2 cm on the bronchial side of the carina. The tube was also located at 2.3 +/- 1.0 cm on the bronchial side of the carina when a unilateral shape of visualized breath sounds was obtained using the Visual Stethoscope (not significant).
During advancement of the tracheal tube, alterations of the shape of the visualized breath sounds using the Visual Stethoscope appeared before the changes of the breath sounds were detected by auscultation. Bilateral breath sounds disappeared when the tip of the tracheal tube was advanced beyond the carina in both groups.
Anesthesia and analgesia 12/2009; 109(6):1836-42. · 3.08 Impact Factor
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ABSTRACT: Hemorrhagic shock increases the hypnotic effect of propofol, but the influence of hemorrhagic shock on the immobilizing effect of propofol is not fully defined.
Twenty-four swine (30.3 +/- 3.6 kg) were anesthetized by inhalation of isoflurane and randomly assigned to either a control (n = 12) or a hemorrhagic shock (n = 12) group. Animals in the shock group were bled to a mean arterial blood pressure of 50 mm Hg and maintained at this level for 60 min. After isoflurane inhalation was stopped, propofol was infused at 50 mg x kg(-1) x h(-1) until no movement was observed after application of a dewclaw clamp every 2 min. Arterial samples for measurement of the propofol concentration were collected just before each use of the dewclaw clamp and the Bispectral Index (BIS) was also recorded. Analysis of the pharmacodynamics was performed using a sigmoidal inhibitory maximal effect model for BIS versus effect-site concentration and a logistic regression analysis for the probability of movement versus effect-site concentration.
The propofol doses needed to reach a 50% decrease from baseline BIS, and no movement after noxious stimuli were reduced by hemorrhagic shock by 54% and 38%, respectively. Hemorrhagic shock decreased the effect-site concentration that produced 50% of the maximal BIS effect from 11.6 +/- 3.8 to 9.1 +/- 1.7 microg/mL and that producing a 50% probability of movement from 26.8 +/- 1.0 to 20.6 +/- 1.0 microg/mL.
The results show that hemorrhagic shock increases both the hypnotic and immobilizing effects of propofol due to pharmacokinetic and pharmacodynamic alterations, with the changes in pharmacodynamics occurring to a similar extent for both effects.
Anesthesia and analgesia 09/2009; 109(2):398-404. · 3.08 Impact Factor
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Pediatric Anesthesia 05/2008; 18(4):339. · 2.10 Impact Factor
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ABSTRACT: Although hemorrhagic shock decreases the minimum alveolar concentration (MAC) of inhaled anesthetics, it minimally alters the electroencephalographic (EEG) effect. Hemorrhagic shock also induces the release of endorphins, which are naturally occurring opioids. We tested whether the release of such opioids might explain the decrease in MAC.
Using the dew claw-clamp technique in 11 swine, we determined the isoflurane MAC before hemorrhage, after removal of 30% of the estimated blood volume (21 mL/kg of blood over 30 min), after fluid resuscitation using a volume of hydroxyethylstarch equivalent to the blood withdrawn, and after IV administration of 0.1 mg/kg of the mu-opioid antagonist naloxone.
Hemorrhagic shock decreased the isoflurane MAC from 2.05% +/- 0.28% to 1.50% +/- 0.51% (P = 0.0007). Fluid resuscitation did not reverse MAC (1.59% +/- 0.53%), but additional administration of naloxone restored it to control levels (1.96% +/- 0.26%). The MAC values decreased depending on the severity of the shock, but the alterations in hemodynamic variables and metabolic changes accompanying fluid resuscitation or naloxone administration did not explain the changes in MAC.
Consistent with previous reports, we found that hemorrhagic shock decreases MAC. In addition, we found that naloxone administration reversed the effect on MAC, and we propose that activation of the endogenous opioid system accounts for the decrease in MAC during hemorrhagic shock. Such an activation would not be expected to materially alter the EEG, an expectation consistent with our previous finding that hemorrhagic shock minimally alters the EEG.
Anesthesia and analgesia 01/2008; 105(6):1639-43, table of contents. · 3.08 Impact Factor
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ABSTRACT: The facial edema and tongue swelling after oral surgery are not rare complications and many case reports were published, but they were limited after anesthesia for surgery of other parts. A 70-year-old woman who had underwent thoraco-abdominal aortic graft surgery showed severe facial edema and tongue swelling after the surgery in the right lateral position. The tongue was largely protruded outside of the mouse when entering ICU and was gradually improved. Twelve hours later, the tongue was shrunken into the mouse. The patient was moved to a general ward without any complications on the 5th postoperative day. The patient had taken anti-hypertensive drugs including candesartan for a long period. She might have become susceptible to angioedema by angiotensin receptor blocker such as angiotensin-converting enzyme inhibitor and stress of surgery, and anesthesia might have induced a complication of the acute tongue swelling. Although, prevention and treatment of angioedema have not been established, careful observation would be required.
Masui. The Japanese journal of anesthesiology 10/2007; 56(9):1100-3.
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Canadian Journal of Anaesthesia 03/2007; 54(2):155-7; author reply 157. · 2.35 Impact Factor
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ABSTRACT: To determine the effect of xenon in combination anesthesia with sevoflurane on the catecholamine and hemodynamic responses to surgical noxious stimulation in humans.
Randomized study.
A university hospital.
This study involved 32 female ASA physical status I and II patients, age 20-58 years, scheduled for abdominal hysterectomy.
Patients were randomly divided into 4 groups: group X50-S1.5, 50% xenon and 1.5% sevoflurane; group X70-S1.5, 70% xenon and 1.5% sevoflurane; group G70-S1.5, 70% nitrous oxide and 1.5% sevoflurane; and group S2.8, 2.8% sevoflurane. No premedication was administered to the patients, and anesthesia was induced by administration of sevoflurane in oxygen and 0.10 to 0.15 mg/kg of vecuronium. After tracheal intubation, the combination of anesthetics was started, and skin incision was performed after equilibration for more than 15 minutes.
Systolic blood pressure and heart rate (HR) were recorded, and the plasma concentrations of norepinephrine, epinephrine (E), and dopamine were measured 0, 2.5, 5, 7.5, 10, 12.5, and 15 minutes after skin incision.
The maximal increase in the E concentration and the values of the area under the curve for E were significantly smaller in the X50-S1.5 and X70-S1.5 groups compared with that in the S2.8 group (P<0.05). At 1 minute after incision, the HR in X50-S1.5 was significantly lower than those in G70-S1.5 and S2.8 groups and the HR in X70-S1.5 was lower than that in S2.8 group (P<0.01). The systolic blood pressure in S2.8 group at 1 minute was significantly higher than those of other groups (P<0.01).
Combination anesthesia using xenon and sevoflurane suppresses the plasma E concentration and hemodynamic response after skin incision more effectively than sevoflurane anesthesia alone.
Journal of Clinical Anesthesia 08/2006; 18(5):343-8. · 1.21 Impact Factor
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ABSTRACT: The properties of two new-generation CO(2) absorbents, Amsorb Plus (Armstrong Medical, Coleraine, UK) and Drägersorb Free (Drager, Lubeck, Germany), were compared with those of Amsorb (Armstrong Medical) and Sodasorb II (W.R. Grace, Lexington, MA, USA).
The concentration of compound A produced by each absorbent was determined in a low-flow circuit containing sevoflurane, and the CO(2) absorption capacity of the absorbent was measured. The circuit contained 1000 g of each absorbent and had a fresh gas (O(2)) flow rate of 1 l.min(-1) containing 2% sevoflurane. CO(2) was delivered to the circuit at a flow rate of 200 ml.min(-1).
The maximum concentrations of compound A were 2.2 +/- 0.0, 2.3 +/- 0.3, 2.2 +/- 0.2, and 23.5 +/- 1.5 ppm (mean +/- SD) for Amsorb Plus, Drägersorb Free, Amsorb, and Sodasorb II, respectively. The maximum concentration of compound A for Sodasorb II was significantly higher than those for the other absorbents (P < 0.01). The CO(2) absorption capacities (time taken to reach an inspiratory CO(2) level of 2 mmHg) were 1023 +/- 48, 1074 +/- 36, 767 +/- 41, and 1084 +/- 54 min, respectively, and the capacity of Amsorb was significantly lower than that of the other absorbents (P < 0.01).
The new-generation carbon dioxide absorbents, Amsorb Plus and Drägersorb Free, produce a low concentration of compound A in the circuit while showing sufficient CO(2) absorption capacity.
Journal of Anesthesia 01/2004; 18(4):277-81. · 0.83 Impact Factor
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ABSTRACT: We compared the ease of passage through the glottis of two different tubes and two different sizes of tracheal tube exchanger (TE) during introducer-guided tracheal intubation. One tube was a polyvinyl chloride tube with a standard bevel, and the other was a newly designed tube with a hemispherical bevel. The outer diameters (OD) of the two TEs were 2.5 and 5.0 mm. After the standard induction of anesthesia, followed by vecuronium-induced paralysis, a TE was inserted into the trachea with a direct laryngoscope. By using the introducer as a guide, the tracheal tube was inserted into the trachea. The difficulty in passing the tube was assessed by a blinded observer and graded with a four-point scale. The newly designed tube was inserted more smoothly than was the conventional tube when the 2.5-mm-OD TE was used (P < 0.01). In situations such as those occurring after one-lung anesthesia, when use of a thicker TE is not applicable, this newly designed taper-tipped tube may be considered as an adjunct to oral tracheal tube exchange, using a thinner (smaller-OD) TE as the guide for tracheal intubation. IMPLICATIONS: In situations such as after one-lung anesthesia, when use of a thicker tube exchanger (TE) is not applicable, a newly designed taper-tipped tube with the leading edge in the midline may be considered as an adjunct to an oral tracheal tube exchange, using a thinner TE as the guide for tracheal intubation.
Anesthesia & Analgesia 07/2003; 97(1):285-8, table of contents. · 3.29 Impact Factor
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ABSTRACT: To determine compound A concentrations in a low-flow circuit containing Drägersorb Free (Dräger, Lübeck, Germany), Amsorb (Armstrong, Coleraine, Northern Ireland), and Sodasorb II (W. R. Grace, Lexington, MA).
Randomized study.
Hamamatsu University Hospital.
24 ASA physical status I and II patients scheduled for general anesthesia greater than 3 hours' duration.
Patients were allocated to three groups of eight patients each to receive either using either Drägersorb Free, Amsorb, or Sodasorb II. Immediately before anesthesia induction, 1 kg of fresh absorbent was placed in the anesthesia canister. Anesthesia was maintained with sevoflurane (end-tidal concentration 1% to 3%) in oxygen and nitrous oxide (FIO(2) > 0.3) at a total flow of 1 L/min.
Inspiratory compound A concentration in the circuit was measured once every hour.
Maximum compound A concentrations for Drägersorb Free, Amsorb, and Sodasorb II were 2.4 +/- 0.8 (mean +/- SD) ppm, 3.1 +/- 0.5 ppm, and 28.0 +/- 10.0 ppm (p < 0.01 vs. Drägersorb Free and Amsorb). Concentrations with Drägersorb Free and Amsorb remained at less than 4 ppm throughout the study.
Because compound A concentrations in the circuit with Drägersorb Free and Amsorb were negligible, sevoflurane can be used at a fresh gas flow of 1 L/min with these two absorbents.
Journal of Clinical Anesthesia 02/2003; 15(1):33-7. · 1.21 Impact Factor
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Journal of Anesthesia 02/2003; 17(2):145-6. · 0.83 Impact Factor
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ABSTRACT: Purpose. CO2 absorbents convert sevoflurane to fluoromethyl-2,2-difluoro-1-(trifluoromethyl) vinyl ether (compound A), whose toxicity
in rats raises concern regarding the safety of sevoflurane in a low-flow system. The type of CO2 absorbent is one of factors that affect compound A concentration in the anesthetic circuit. The aim of the present study
was to investigate the concentration of compound A in an anesthetic model circuit following the use of different brands of
soda lime and Baralyme.
Methods. We measured the concentrations of compound A in four different brands of CO2 absorbent using a low-flow (1 l·min−1 fresh gas) model circuit in which 2% sevoflurane was circulated. Sodasorb II, Baralyme, Sofnolime and Wakolime-A were used
as CO2 absorbents. The concentration of compound A was measured hourly, and the temperature of the CO2 absorbent was monitored.
Results. The maximum concentration of compound A in the circuit was highest for Baralyme (25.5 ± 0.6 ppm) (mean ± SD), followed by
Sodasorb II (18.9 ± 1.6 ppm), Wakolime-A (16.1 ± 0.7 ppm), and Sofnolime (15.8 ± 1.4 ppm). The maximum temperature was 50.8
± 1.3°C for Baralyme, 48.8 ± 1.3°C for Wakolime-A, 47.0 ± 1.4°C for Sodasorb II, and 43.5 ± 3.9°C for Sofnolime.
Conclusion. The relative concentrations of compound A in the low-flow circuit were Baralyme > Sodasorb II > Wakolime-A = Sofnolime.
Journal of Anesthesia 06/2000; 14(3):143-146. · 0.83 Impact Factor
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ABSTRACT: Background: Fentanyl produces a reduction in the minimum alveolar concentration (MAC) of isoflurane and desflurane needed to blockade adrenergic response (BAR) to surgical incision in 50% of patients (MAC‐BAR). MAC‐BAR of sevoflurane and the reduction in MAC‐BAR of sevoflurane by fentanyl have not been described previously. The purpose of this study was to determine the MAC and MAC‐BAR reduction of sevoflurane by fentanyl with and without nitrous oxide (N2 O).
Anesthesiology 01/1999; 90(2):398–405. · 5.36 Impact Factor
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ABSTRACT: It has been reported that the actual flow from a syringe pump changes due to vertical movement of the pump in vitro, but a direct study of the in vivo effects of fluid delivery irregularities caused by vertical pump displacement has not been performed. The aim of this study was to assess the influence of positional changes of the syringe pump on the internal pressure (IP) and flow from the circuit, and to examine blood pressure changes caused by pump movement in animals with or without hemorrhagic shock.
To simulate clinical conditions, we used a rabbit model. We first measured the changes in line IP and flow from the syringe pump after moving the pump 50 cm vertically upwards or downwards. With the same animal, we then recorded the blood pressure changes under these conditions during norepinephrine (NE) infusion, using a rabbit hemorrhagic shock (HS) model.
Following downward movement of the syringe pump, the IP increased by 37.5 +/- 4.0 mmHg and IP decreased by 37.3 +/- 3.1 mmHg following upward movement of the syringe pump. In the rabbit HS model, movement downwards decreased systolic blood pressure (SBP) by -17 +/- 6.9% (P < 0.001), while upward movement raised SBP by 45.7 +/- 21.5% (P < 0.001) from baseline values.
Vertical displacement of the syringe pump alters the flow due to a change of line IP, and blood pressure can be affected by pump movement during NE infusion.
Canadian Journal of Anaesthesia 52(7):685-91. · 2.35 Impact Factor
