To investigate the effects of ketamine on nitric oxide synathase(NOS)activity, nitrc oxide (NO) output and cyclic guanosine 3', 5'-monophosphate(cGMP)content in the rat brain. Method: Thirty two SD rats were divided randomly into control group and ketamine group. The aminals were administred intraperitoneally(ip)normal saline 10mg?kg~(-1) or ketamine 100mg?kg~(-1), respectively. NOS activity and NO output were assassed with spectrophotometric analysis, cGMP content was measured with radioimmunoassay, Result: Ketamine 100mg?kg~(-1) ip significantly inhibited NOS activity(P

Tn investigate the effects of propofol on Ca~(2+) ATPase activity in rat cerebral synaptic membrane. Method: Thirty SD rats were divided randomly into three groups. The aminals were administtered introperi toneally(ip) propofol 50mg?kg~(-1), 100mg?kg~(-1) or normal saline 10mg?kg~(-1)(control group), respectively. These rats were immediately decapitated after having disappeared righting reflex. In oredr to prepare synaptosomes, brain tissues were dissected on ice, then homogenized and centrifuged. Ca~(2+)-ATPase activity was assaed with spcetrophotometric analysis. Result: Propofol 100mg?kg~(-1) ip significantly inhibited Ca~(2+)-ATPase activity of cerebrocortical, brain stems and hippocampal synaptic membrane as compared with that of normal saline group(P

Objective:To investigate effects of propofol on nitric oxide synthase (NOS) activity and nitric oxide (NO)output of rat brain. Method: Sixteen SD rats were divided randomly into two groups. The animals were administered introperitoneally(ip) normal saline 10 ml?kg~(-1)(control group)or propofol 100mg?kg~(-1)(propofolgroup),respectively. These rats were decapitated immediately after having disappeared righting reflex. After rapid removal of cerebellum, brain stem,hippocampus and cerebral cortex,tissues were homogenized and centrifuged. NOS activity and NO output were assayed with spectrophotometric analysis. Result: In propofol group,NOS activity was significantly inhibited, NO outpul was significantly reduced in cerebellum, brain stem,hippoeampus and cerebral cortex as compared with those of control group(P

Objective:To investigate the effects of enflurane on antioxidant ability in ischemic preconditioned rat hearts in vitro. Method:Ninety-six SD rat hearts were perfused with Langendorff device. All hearts were randomly allocated to four groups:Control, enflurane group receiving 40 min of enflurane (1.5MAC),ischemic preconditioning group undergoing two 5-min ischemia and 10-min reperfusion, enflurane + ischemia group receiving enflurane (1.5MAC) for 10 min before ischemia preconditioning procedures. All groups underwent 25-min ischemia and 30-min reperfusion. Left ventricular pressure (LVP), heart rats (HR)and ischemic contracture pressure (ICP) were monitored. Myocardial superoxide dismutase(SOD)and malodialdehyde(MDA)were measured before ischemia, 15min following ischemia and 30 min following reperfusion. Result: Treated groups had better myocardial functional recovery of contractility compared to control groups,with preconditioning being better than enflurane (P

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.

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.

0.05).Inside experimental area,pain scores were decreased in both intradermal 0.25% lidocaine and saline injection group(P

Objective To compare the effects of combined general-epidural anesthesia (CGEA) and general anesthesia (GA) on energy metabolism and oxygen cost of breathing.Methods Forty patients (25 male, 15 female) aged 42-61 yr weighing 42-75 kg scheduled for elective upper abdominal surgery were randomly divided into 2 groups : group CGEA (Ⅰ, n = 20) and group GA (Ⅱ, n = 20) . The patients were premedicated with midazolam 0.05 mg?kg-1 and scopolamine 0.3 mg i.m. . In groupⅠepidural catheter was placed at T9-10 A. test dose of 4ml of 2 % lidocaine was given. When the height of block was confirmed general anesthesia was started. In both groups anesthesia was induced with etomidate 0.3 mg?kg-1 , fentanyl 8 ?g?kg-1 and tracheal intubation was facilitated with atracurium 0.8 mg?kg-1 . Anesthesia was maintained with propofol in both group and intermittent epidural lidocaine in CGEA group and intermittent i. v. boluses of fentanyl in GA group. Muscle relaxation was maintained with atracurium infusion at 8 ?g?kg-1 ? min-1 during operation. Oxygen consumption ( VO2 ), CO2 production (VCO2 ) , energy expenditure ( EE) and respiratory quotient (RQ) were measured before anesthesia, during and after operation using indirect calorimetry (Datex, Deltatrac MBM-200) . Postoperative oxygen cost of breathing (OCB) was calculated during spontaneous breathing and controlled ventilation. Results VO2 , VCO2 , EE were significantly lower and RQ was significantly higher during operation than those before anesthesia in both groups (P

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

Aim To explore the effect of propofol preconditioning on cardiocyte apoptosis and cytochrome C release from mitochondria during hypoxia/reoxygenation in isolated rat hearts.Methods Fifty male Sprague-Dawley rats weighing 250～300 g were randomly divided into 5 groups(n=10 each):control group(C);Dimethyl sulfoxide(DMSO)preconditioning group(D);3 propofol preconditioning groups with 25 ?mol?L-1(P1)、50 ?mol?L-1(P2)、100 ?mol?L-1(P3)propofol respectively.The isolated rat hearts were retrogradely perfused via aorta with K-H solution on Langendorff apparatus.The isolated hearts were made hypoxia for 30 minutes followed by 60 minutes reoxygenation in each group.The D,P1,P2,P3 groups were preconditioned by perfusing 10 min K-H solution containing 20 ?mol?L-1 DMSO and 25,50,100 ?mol?L-1 propofol respectively and then followed by 5 min K-H solution reperfusion before hypoxia.The preconditioning procedure was repeated twice.The cardiac functional variables were recorded after equilibration(baseline values),immediately before hypoxia,at the end of 30 min and 60 min reoxygenation.Apoptotic myocardial cells were detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling(TUNEL)and the level of cytochrome C expression in myocardial cytosol and mitochondria was measured by Western blot at the end of reoxygenation.Results At the end of 30 min and 60 min reoxygenation,LVEDP was significantly lower and LVDP was significantly higher in P1,P2,P3 groups than in D group(P