Objective: To study the effects of halothane and sevoflurane on myocardial function and energy metabolism. Method:The model of Langendorff perfused isolated rat heart was used to investigate the effects of halothane and sevoflurane on HR,LVEDP,LVDP,+dp/dt,-dp/dt and coronary flow(CF)before and after ischemia. and the myocardial ATP content were measured with HPLC before ischemia and 10 min after ischemia and at the end of reperfusion. Result: 1.5 MAC sevoflurane significantly increased CF in normal isolated rat hearts. Both halothane and sevoflurane differently depressed myocardial contratile function,increased normal myocardial energy storage. At 10th min of ischemia the decrease of myocardial ATP content was delayed by halothane and sevoflurane. At the end of reperfusion,the both anesthetics improved the recovery of myocardial function and matebolism,especially sevoflurane. Conclusion: Both anesthetics can protect myocardium from ischemic reperfusion injury through improving post-ischemic myocardial energy recovery.

0 05) Conclusion The cardiotoxicity of ropivacaine is related to the inhibition of sodium and calcium channels

Currently hypothermia neuroprotection is one of the study topics of general interest. The studies of therapeutic hypothermia for acute stroke are increasingly arousing general concern. This article reviews the mechanism of therapeutic hypothermia for acute stroke, the effect of increased body temperature on acute stroke, and the clinical application of therapeutic hypothermia for acute stroke.

Aim To investigate the role of peripheral benzodiazepine receptor in rat cardiac mitochondrial permeability transition.Methods The isolated rat cardiac mitochondria were incubated with different doses(50,100,200 ?mol?L-1) of PBR antagonist 1-(2-chlorophenyl-N-methyl-1-methylpropyl)-3-isoquinolinecarboxamide (PK 11195). In additional group(CsA group), 5 ?mol?L-1 cyclosporine A (CsA), an inhibitor of MPT was added 5 minutes before the addition of 100 ?mol?L-1 PK 11195. Negative control group(Con group) was given none treatment. Positive control group(Ca2+ group) was given 150 ?mol?L-1 CaCl2. The absorbanceat 520 nm(Abs 520 nm) was monitored with a split-beam spectrophotometer at 30℃ for 10 min. The mitochondrial ultrastructure was assessed by transmission electron microscopy. Mitochondrial cytochrome C release was demonstrated by Western Blotting.Results PK11195 triggered large-amplitude mitochondrial swelling in a dose dependent manner(vs Con group,P

Objective To investigate the expression of apoptosis-related genes Bcl-2 and Bax after cerebral ischemic reperfusion in hippocampal CA1 and CA3 areas and the effect of curcumin on the expression of Bcl-2 and Bax in gerbils.Methods Gerbils were randomly divided into sham group(SH),ischemia-reperfusion group(IR),curcumin group(CU) and solvent control group(SC).Forebrain ischemia was induced by occlusion of bilateral common carotid arteries.Observations were made in each group 1d,3d,5d and 7d after ischemia.Open field test was used to examine the behavioral change.The apoptotic neurons in hippocampal CA1 region was counted,and the expression of Bcl-2 and Bax in hippocampal CA1 and CA3 areas was detected by SABC immunocytochemical technique.Results The behavioral mark and the number of apoptotic neurons in hippocampal CA1 and CA3 areas were much smaller in CU group than in IR group(P

0.05); in hot-plate test , strychnine at 0.1,0.2,0.4 ?g (it) can significantly and dose dependently decrease the HPPI of the mice treated with aether,enflurane and sevoflurane (P0.05), but at 0.2,0.4 ?g (it) could significantly decrease the HPPI of mice treated with isoflurane(P

Aim To investigate the relationship between neuronal nicotinic acetylcholine receptor and the amnesia and hypnosis induced by enflurane in mice.Methods Animal models were established by Intraperitoneal injecting of enflurane(2.2 ml?kg-1 and 0.4 ml?kg-1).Artificial cerebrospinal fluid or different dose of nicotine were intracerebroventricular injected,then sleeping time in the analeptic test was recorded;and the step down latency and error times in the step down test;step through latency and error times in the step through test.For the independent activity test,recorded the independent activity times of mice treated with enflurane(0.4 ml?kg-1) in 5 min.Results Compared with control group,intracerebroventricular nicotine decreased sleeping time in the analeptic test,increased step down latency and step through latency in both step down test and step through test.Furthermore,the error times were decreased in both tests.All the outcomes were significant and the influence was dose-dependent.There was no significant difference for the independent activity times of mice treated with 0.4 ml?kg-1 enflurane by ip injection.Conclusion All the evidence suggested that neuronal nicotinic receptor is one of important targets for the hypnotic and amnestic effect of enflurane in mice.

Aim To establish a method to quantitatively determine cardiolipin content and investigate effects of age and ischemia on cardiolipin in isolated rat hearts.Methods Male SD rats, 4 months old,12 months old and 24 months old were used throughout the experiment. Each had 24 ones,which were randomly distributed to control,ischemia 30 min and ischemia 40 min groups(n=8). Control group hearts were perfused for a total of 70 min and ischemia groups hearts were perfused for a 20 min equilibration period,and then underwent 30 or 40 min of no-flow ischemia followed by reperfusion for a 20 min period, respectively.Cardiolipin was quantitatively determined by high-performance liquid chromatography following extraction of lipids from subsarcolemmal mitochondria(SSM)and interfibrillar mitochondria(IFM).Results Under the condition of HPLC,the retention time of cardiolipin was 13.092 min. The standard curve was Y^ (?V?s) =20 877 455X(mmol?L-1)-352 028(r=0.9993) with a validated quantitation range of 0.2～3.2 mmol?L-1,and the lowest concentration of detection was 0.005 mmol?L-1 (S/N=3). At the concentration of 0.2,0.8,3.2 mmol?L-1,absolute recovery rates ranged from 0.8505 to 0.9519 and relative recovery rates ranged from 0.9898 to 1.0429. The RSD of the precision within-day and between-day was less than 0.11. Cardiolipin content in SSM of nonischemic group of 24 months old rats was lower than that of both 4 months old and 12 months old, but no differences among them were observed in IFM.In all age rats, compared with control group,cardiolipin contents of SSM from ischemia 30 min and ischemia 40 min groups were lower, and effects of ischemia 40 min are not pronounced; there were no differences in CL contents of IFM among three groups.Conclusions The assay method was shown to be sensitive, suitable and accurate for determination of cardiolipin located in mitochondria from perfused hearts of rats. Myocardial ischemia and older age decreased cardiolipin content in SSM, and had no remarkable effects on cardiolipin in IFM.

0.05).After reperfusion,Sevo group and Post group resulted in a significant increase(P

Aim To investigate whether endogenous hydrogen sulfide participated in the ischemic postconditioning against ischemia/reperfusion injury in the isolated rat hearts.Methods Isolated SD rat hearts were subjected to ischemia by stopping perfusion for 30 min followed by reperfusion for 60 min in Langendorff perfusion system,at the onset of reperfusion,4 cycles of 15 seconds reperfusion followed by 15 seconds ischemia were given for postconditioning.Intraperitoneal injection of L-propargylglycine(PAG,the inhibitor of cystanthionine-?-lysase) half an hour before operation or administration of exogenous hydrogen sulfide donor-NaHS for postconditioning was performed to observe the impact on ischemic postconditioning.The heart rate(HR),left ventricular developed pressure(LVDP),coronary arterial flow(CF)were recorded.The activity of lactate dehydrogenase(LDH)in the coronary effluent fluid,and the activity of CSE and the content of H2S in the isolated rat hearts were measured with colorimetry method.The infarction sizes were measured with TTC dying method.Results In ischemic/reperfusion group,LVDP decreased,the activity of LDH in the coronary effluent fluid and the size of myocardial infarction increased(vs control,P