Objective To investigate the protective effects of emulsified isoflurane induced preconditioning on ischemia-reperfusion injury in rabbit hearts in vivo. Methods Thirty-two healthy rabbits of male weighing 2 kg2.5 kg ...Objective To investigate the protective effects of emulsified isoflurane induced preconditioning on ischemia-reperfusion injury in rabbit hearts in vivo. Methods Thirty-two healthy rabbits of male weighing 2 kg2.5 kg were anesthetized with intramuscular Ketamine 70 mg/kg. The animals PaCO2 was maintained at 35 mmHg45 mmHg.The animals were randomly allocated to one of 4 groups of 8 animals in each group:control group received no pretreatment（C）;and three groups were pretreated with lipid vehicle（L）,isoflurane（I） and emulsified isofiurane（EI）. Each group was subjected to 1 h occlusion of left anterior descending artery followed by 3 h reperfusion. The change of haemodynamics parameters was observed. Results There were no statistically significant different in HR,MAP,cardiac output （CO）,left ventricular systolic pressure（LVSP）,the maximum rate of left ventricular systolic pressure（+dp/dtmax ）,left ventricular end-diastolic pressure（LVEDP）and rate-pressure products（RPP） among all groups during ischemia and early reperfusion period. LVSP in control group and lipid vehicle pretreatment proup were much lower while LVEDP higher than that in all precondition proups during the late reperfusion period（P<0.05）,the other haemodynamics parameters were no statistically significant different（P>0.05）.Conclusion Emulsified isoflurane-induced preconditioning as isoflurane significant myocardial protection against ischima-reperfusion injury in vivo rabbit hearts.展开更多
Objective To investigate the ability of once and twice isoflurane preconditioning against oxygen and glucose deprivation（OGD） injury in rats brain in vitro.Methods Rat hippocampal slices were exposed to 1vol%,2vol% ...Objective To investigate the ability of once and twice isoflurane preconditioning against oxygen and glucose deprivation（OGD） injury in rats brain in vitro.Methods Rat hippocampal slices were exposed to 1vol%,2vol% and 3vol% isoflurane for 30 min under normoxic condition（95% O2/5% CO2） once and twice（n=12 for each group） respectively before OGD.At the end of each exposure,the slices were set with a 15-min washout period interspersed,then slices were exposed to 13-min OGD period（95% N2/5%CO2,glucose-free） followed by 30min reoxygenation.The amplitude CA1 population spikes（PS,neuronal function） was measured and used to quantify the degree of recovery of neuronal function at post OGD period.To assess the role of the mitogen-activated protein kinases（MAPKs） in preconditioning,U0126,an inhibitor of extracellular signal-regulated protein kinase（MEK-ERK1/2）,and SB203580,an inhibitor of p38 MAPK,were used during isoflurane exposure.Results Isoflurane-preconditioning with 1vol%,2vol% and 3vol% once increased the degree of recovery from 4.8%±1.4%（control） to 41.9%±9.2%,55.1%±11.0% and 63.2%±10.8%,respectively,and twice to 53.8%±12.0%,63.5%±11.1% and 76.3%±12.3%, respectively.The effect of twice exposure to 3vol% isoflurane was blocked by U0126（6.1%±1.5%）.Conclusion It is concluded that twice isoflurane preconditioning could achieve better neuroprotection than once via activation of extracellular signal-regulated protein kinase（MEK-ERK1/2）.展开更多
Objective To test the ability of isoflurane-induced preconditioning against oxygen and glucose dep- rivation （OGD） injury in vitro. Methods Rat hippocampal slices were exposed to 1 volume percentage （vol%）, 2vo1%...Objective To test the ability of isoflurane-induced preconditioning against oxygen and glucose dep- rivation （OGD） injury in vitro. Methods Rat hippocampal slices were exposed to 1 volume percentage （vol%）, 2vo1% or 3vo1% isoflurane respectively for 20 minutes under normoxic conditions （95% O2/5% CO2） once or twice （12 slices in each group） before OGD, with 15-minute washout after each exposure. During OGD experiments, hippocampus slices were bathed with artificial cerebrospinal fluid （ACSF） lacking glucose and perfused with 95% N2 and 5% CO2 for 14 minutes, followed by a 30-minute reperfusion in normal ACSF. The CA1 population spike （PS） was measured and used to quantify the degree of neuronal function recovery after OGD. To assess the role of mitogen-activated protein kinases （MAPKs） in isoflurane preconditioning, U0126, an inhibitor of extracellular signal-regulated protein kinase （ERK1/2）, and SB203580, an inhibitor of p38 MAPK, were used before two periods of 3vol% isoflurane exposure. Results The degree of neuronal function recovery of hippocampal slices exposed to 1 vol%, 2vol%, or 3vol% isoflurane once was 41.88%±9.23%, 55.05%±11.02%, or 63.18%±10.82% respectively. Moreover, neuronal function recovery of hippocampal slices exposed to 1 vol%, 2vo1%, or 3vo1% isoflurane twice was 53.75%±12.04%, 63.50%±11.06%, or 76.25%±12.25%, respectively. Isoflurane preconditioning increased the neuronal function recovery in a dose-dependent manner. U0126 blocked the preconditioning induced by dual exposure to 3vo1% isoflurane （6.13%±1.56%, P〈0.01） and ERK1/2 activities. Conclusions Isoflurane is capable of inducing preconditioning in hippocampal slices in vitro in a dose-dependent manner, and dual exposure to isoflurane with a lower concentration is more effective in triggering preconditioning than a single exposure. Isoflurane-induced neuroprotection might be involved with ERK 1/2 activities.展开更多
Objective： We compare the cardioprotective effects of anesthetic preconditioning by propofol and/or isoflurane in rats with ischemia-reperfusion injury. Methods： Male adult Wistar rats were subjected to 60 min of an...Objective： We compare the cardioprotective effects of anesthetic preconditioning by propofol and/or isoflurane in rats with ischemia-reperfusion injury. Methods： Male adult Wistar rats were subjected to 60 min of anterior descending coronary artery occlusion followed by 120 rain of reperfusion. Before the long ischemia, anesthetics were administered twice for 10 min followed by 5 min washout. Isoflurane was inhaled at 1 MAC （0.016） in I group, whereas propofol was inhaled intravenously at 37.5 mg/（kg.h） in P group. A combination ofisoflurane and propofol was administered simultaneously in I＋P group. Results： In control （without anesthetic preconditioning, C group）, remarkable myocardial infarction and apoptosis accompanied by an increased level of cardiac troponin T were noted 120 min aider ischemia-reperfusion. As compared to those of control group, I and P groups had comparable cardioprotection. In addition, I＋P group shares with I and P groups the comparable cardioprotective effects in terms of myocardial infarction and cardiac troponin T elevation. Conclusion： A combination of isoflurane and propofol produced no additional cardioprotection.展开更多
基金Supported in part by grant Nos.HL 034708 (to Dr. Bosnjak) PO1 GM066730 (to Dr. Bosnjak) from the National Institutes of Health+1 种基金 Bethesda Maryland.
文摘Objective To investigate the protective effects of emulsified isoflurane induced preconditioning on ischemia-reperfusion injury in rabbit hearts in vivo. Methods Thirty-two healthy rabbits of male weighing 2 kg2.5 kg were anesthetized with intramuscular Ketamine 70 mg/kg. The animals PaCO2 was maintained at 35 mmHg45 mmHg.The animals were randomly allocated to one of 4 groups of 8 animals in each group:control group received no pretreatment（C）;and three groups were pretreated with lipid vehicle（L）,isoflurane（I） and emulsified isofiurane（EI）. Each group was subjected to 1 h occlusion of left anterior descending artery followed by 3 h reperfusion. The change of haemodynamics parameters was observed. Results There were no statistically significant different in HR,MAP,cardiac output （CO）,left ventricular systolic pressure（LVSP）,the maximum rate of left ventricular systolic pressure（+dp/dtmax ）,left ventricular end-diastolic pressure（LVEDP）and rate-pressure products（RPP） among all groups during ischemia and early reperfusion period. LVSP in control group and lipid vehicle pretreatment proup were much lower while LVEDP higher than that in all precondition proups during the late reperfusion period（P<0.05）,the other haemodynamics parameters were no statistically significant different（P>0.05）.Conclusion Emulsified isoflurane-induced preconditioning as isoflurane significant myocardial protection against ischima-reperfusion injury in vivo rabbit hearts.
文摘Objective To investigate the ability of once and twice isoflurane preconditioning against oxygen and glucose deprivation（OGD） injury in rats brain in vitro.Methods Rat hippocampal slices were exposed to 1vol%,2vol% and 3vol% isoflurane for 30 min under normoxic condition（95% O2/5% CO2） once and twice（n=12 for each group） respectively before OGD.At the end of each exposure,the slices were set with a 15-min washout period interspersed,then slices were exposed to 13-min OGD period（95% N2/5%CO2,glucose-free） followed by 30min reoxygenation.The amplitude CA1 population spikes（PS,neuronal function） was measured and used to quantify the degree of recovery of neuronal function at post OGD period.To assess the role of the mitogen-activated protein kinases（MAPKs） in preconditioning,U0126,an inhibitor of extracellular signal-regulated protein kinase（MEK-ERK1/2）,and SB203580,an inhibitor of p38 MAPK,were used during isoflurane exposure.Results Isoflurane-preconditioning with 1vol%,2vol% and 3vol% once increased the degree of recovery from 4.8%±1.4%（control） to 41.9%±9.2%,55.1%±11.0% and 63.2%±10.8%,respectively,and twice to 53.8%±12.0%,63.5%±11.1% and 76.3%±12.3%, respectively.The effect of twice exposure to 3vol% isoflurane was blocked by U0126（6.1%±1.5%）.Conclusion It is concluded that twice isoflurane preconditioning could achieve better neuroprotection than once via activation of extracellular signal-regulated protein kinase（MEK-ERK1/2）.
基金Supported by Foundation of Shihezi University of Xinjiang Province (RCZX200688)
文摘Objective To test the ability of isoflurane-induced preconditioning against oxygen and glucose dep- rivation （OGD） injury in vitro. Methods Rat hippocampal slices were exposed to 1 volume percentage （vol%）, 2vo1% or 3vo1% isoflurane respectively for 20 minutes under normoxic conditions （95% O2/5% CO2） once or twice （12 slices in each group） before OGD, with 15-minute washout after each exposure. During OGD experiments, hippocampus slices were bathed with artificial cerebrospinal fluid （ACSF） lacking glucose and perfused with 95% N2 and 5% CO2 for 14 minutes, followed by a 30-minute reperfusion in normal ACSF. The CA1 population spike （PS） was measured and used to quantify the degree of neuronal function recovery after OGD. To assess the role of mitogen-activated protein kinases （MAPKs） in isoflurane preconditioning, U0126, an inhibitor of extracellular signal-regulated protein kinase （ERK1/2）, and SB203580, an inhibitor of p38 MAPK, were used before two periods of 3vol% isoflurane exposure. Results The degree of neuronal function recovery of hippocampal slices exposed to 1 vol%, 2vol%, or 3vol% isoflurane once was 41.88%±9.23%, 55.05%±11.02%, or 63.18%±10.82% respectively. Moreover, neuronal function recovery of hippocampal slices exposed to 1 vol%, 2vo1%, or 3vo1% isoflurane twice was 53.75%±12.04%, 63.50%±11.06%, or 76.25%±12.25%, respectively. Isoflurane preconditioning increased the neuronal function recovery in a dose-dependent manner. U0126 blocked the preconditioning induced by dual exposure to 3vo1% isoflurane （6.13%±1.56%, P〈0.01） and ERK1/2 activities. Conclusions Isoflurane is capable of inducing preconditioning in hippocampal slices in vitro in a dose-dependent manner, and dual exposure to isoflurane with a lower concentration is more effective in triggering preconditioning than a single exposure. Isoflurane-induced neuroprotection might be involved with ERK 1/2 activities.
文摘Objective： We compare the cardioprotective effects of anesthetic preconditioning by propofol and/or isoflurane in rats with ischemia-reperfusion injury. Methods： Male adult Wistar rats were subjected to 60 min of anterior descending coronary artery occlusion followed by 120 rain of reperfusion. Before the long ischemia, anesthetics were administered twice for 10 min followed by 5 min washout. Isoflurane was inhaled at 1 MAC （0.016） in I group, whereas propofol was inhaled intravenously at 37.5 mg/（kg.h） in P group. A combination ofisoflurane and propofol was administered simultaneously in I＋P group. Results： In control （without anesthetic preconditioning, C group）, remarkable myocardial infarction and apoptosis accompanied by an increased level of cardiac troponin T were noted 120 min aider ischemia-reperfusion. As compared to those of control group, I and P groups had comparable cardioprotection. In addition, I＋P group shares with I and P groups the comparable cardioprotective effects in terms of myocardial infarction and cardiac troponin T elevation. Conclusion： A combination of isoflurane and propofol produced no additional cardioprotection.
