Objective: To investigate ketamine cardiotoxicity profile. Method:Four day-old spontaneously contracting neonatal primary myocardial cell cultures obtained from 2-to 3-day-old Wistar rats were divided into 4 groups, group A as control and group B,C and D treated with ketamine(1?10~(-5), 1?10~(-4)and 1?10~(-3)mol/L)for 2 to 24 h. The contractility, morphology,cytoplasmic enzyme (LDH, AST and CK) release content of myocardial cell and the concentration of electrolytes (k~+, Na~+, Ca~(2+) and Cl~-) in the medium were measured 2,4,8 and 24 h following ketamine administration. Result:In group B the beating rates of neonatal myocardial cell cultures increased (P

Objective To investigate the relationship between gastric tonometer and stomach tube methods for determining gastrointramucosal pH (pHi) during the operation. Methods General anesthesia was induced in thirty patients. After endotracheal intubation,electrocardiography, blood pressure,HR and SpO 2 were monitored . The gastric juice were collected by the gastric tonometer and stomach tube methods to determine the PCO 2 at 30,60 and 120 min following anesthesia respectively, and at the same time the arterial blood samples were taken to measure the HCO- 3 concentration with American Corning automatic blood-gas and eletrolytes analyzer.Intramucosal pH was calculated using Henderson-Hasselbalch equation. Results Through correlation and regression analysis , there were positive correlations in the pHi determined at three time points between gastric tonometer and stomach tube methods(r=0.699, 0805 and 0792, P

Objective To detemine the effects of ketamine on c-fos gene expression during global myocardial ischemia-reperfusionMethods Forty Wistar rats were divided into 5 groups: group C as control; group CR as ischemia-reperfusion control and group KH,KM and KL treated with ketamine 1?10 -3,1?10 -4 and 1?10 -5mol/L respectively prior to ischemia-reperfusion Total cellular RNA of myocardium was extracted RT-PCR technique was applied to determining cDNA amplification products ?-actin mRNA served as an internal control Densities of DNA bands were quantified using computer image analysis systemResults As compared with the values of group C, c-fos mRNA levels were increased in group CR,KH,KM and KL(P005)Conclusions C-fos gene may involves in molecular modulation of myocardial ischemia-reperfusion injury and myocardial protection Ketamine can effectively depress the expression of c-fos gene in myocardium, the middle and the low concentrations of ketamine are more effective than the high concentrations

Objective To investigate the effect of propofol on apoptosis and expression of Bcl-2 protein induced by myocardial ischemia-reperfusion injury in isolated rat heart. Methods Thirty-six Wistar rats of both sex weighing 250-300 g were anesthetized with intraperitoneal 3% pentobarbital 30 mg?kg-1 . Their hearts were excised and passively perfused with oxygenated (95% O2, 5% CO2) Krebs-Hensleit buffer (KHB) at 37℃ in a Langendorff apparatus. The animals were randomly divided into control and propofol groups. In control group the cannula connecting aorta was cross-clamped for 30 min to induce global ischemia of the isolated heart, followed by 30 min reperfusion. In propofol group the isolated heart was first perfused with KHB containing propofol 10?mol?L-1 for 30 min. Myocardial apoptosis and Bcl-2 protein expression were detected before ischemia, at the end of 30 min ischemia and at the end of 30 min reperfusion in both groups, using TUNEL and immunohistochemical technique.Results Apoptosis index (AI) was significantly increased, while optical density(OD) of Bcl-2 protein was significantly decreased after ischemia and ischemia - reperfusion in both groups as compared with those before ischemia( P

Objective To determine the effects of propofol on c fos gene expression in the different brain regions following stress in rats Methods Twenty one male Wistar rats (12 18 weeks) weighing 260 300g were randomly divided into three groups of seven animals each: control group(C); electrical stimulation group(S) and propofol group(P) The animals were anesthetized with pentobarbital sodium 40mg?kg -1 Normal saline 2ml (group C and S) or propofol 10mg?kg -1 (group P) was injected intraperitoneally (ip) 5 min after ip injection hindpaw of the animals in group S and P was electrically stimulated with 2 mA direct current (1 s every 30 s) for 15 min 30 min after electrical stimulation the animals were decapitated and brain was immediately removed on -20℃ ice plate and kept in -70℃ liquid nitrogen for determination of c fos mRNA expression in cerebral cortex, hypothalamus and hippocampus At the same time 4 ml of blood was collected from trunk for determination of ACTH and cortisol concentrations by immunoradiometric assay Results Plasma ACTH and cortisol levels and c fos mRNA expression in cerebral cortex, hypothalamus and hippocampus increased significantly in group S as compared with those in group C (P0 05).Conclusions The c fos gene is involved in molecular modulation of stress responses Propofol produces different effects on c fos gene expression in different brain regions

Objective To study the protective effects of propofol on isolated rat heart during global myocardial ischemia-reperfusion. Methods 36 Wistar rats were randomly divided into control group and propofol group. Each group was subdivided into 3 subgroups: preischemia, ischemia 30 minutes and ischemia-reperfusion 30 minutes group. The changes in c-fos protein and c-fos mRNA level in isolated Langendorff perfused rat myocardium were assessed by immunohistochemical technique and RT-PCR technique respectively. Results Compared to preischemia subgroup the expression of c-fos protein and c-fos mRNA level in ischemia 30 minutes and ischemia-reperfusion 30 minutes subgroups were higher significantly (P

AIM:The direct renin inhibitor aliskiren displays antihypertensive and antialbuminuric effects in humans and in animal models . Emerging evidence has shown that aliskiren localizes and persists in medullary collecting ducts even after treatment was discontinued . The purpose of the present study was to investigate whether aliskiren regulates renal aquaporin expression and improves urinary concen -trating defect induced by lithium .METHODS:The mice were either fed with normal chow or LiCl diet (40 mmol/kg dry food per day for first 4 days and 20 mmol/kg dry food per day for last 3 days ) for seven days .Some mice were intraperitoneally injected aliskiren ( 50 mg/kg BW per day in saline ) .RESULTS:Mice injected aliskiren developed decreased urine output and increased urine osmolal -ity when compared with controls .Aliskiren significantly increased protein abundance of AQP 2 and phosphorylated-S256 AQP2 in the kidney inner medulla .Immunohistochemistry and immunofluoresence showed increased apical and intracellular labeling of AQP 2 and pS256-AQP2 in collecting duct principal cells of kidneys in mice treated with aliskiren .Aliskiren treatment prevented urinary concen-trating defect in lithium-treated mice , and improved the downregulation of AQP 2 and pS256-AQP2 protein abundance in inner medulla of the kidney .In primary cultured rat inner medulla collecting duct cells , aliskiren dramatically increased AQP 2 protein abundance which was significantly inhibited either by PKA inhibitor H 89 or by adenylyl cyclase inhibitor MDL 12330, indicating an involvement of the cAMP signalling pathway in mediating aliskiren-induced increased AQP 2 expression .CONCLUSION: The direct renin inhibitor aliskiren upregulates AQP 2 protein expression in inner medullary collecting duct principal cells and prevents lithium -induced nephro-genic diabetes insipidus ( NDI) likely via PKA-cAMP pathways .

Objective To evaluate the effect of sevoflurane on myocardial injury induced by hemorrhagic shock and resuscitation (HS/R) in pigs.Methods Twenty-four Bama miniature pigs (12 males, 12 females) , weighing 20-25 kg, aged 3-5 months, were randomly divided into 3 groups (n=8 each) using a random number table: sham operation group (group S) , HS/R group and sevoflurane group (group Sev).The left and right femoral arteries and right femoral vein were cannulated for blood pressure monitoring, blood-letting, blood sampling and fluid infusion.HS/R was induced by blood-letting maintaining for 1 h, followed by resuscitation with autologous blood reinfusion and infusion of lactated Ringer's solution 2 times the volume of the blood withdrawn.The pigs in group Sev were exposed to 2％ sevoflurane for 30 min before resuscitation.After cannulation, at 30 min after hemorrhagic shock, before resuscitation, and at 30 min, and 1.5, 2.5 and 3.5 h after resuscitation, blood samples were collected from the femoral artery for determination of creatine kinase-MB (CK-MB) activity and cardiac troponin Ⅰ (cTnI) concentration in serum using an automatic biochemical analyzer.Myocardial specimens were obtained at 3.5 h after resuscitation for detection of tumor necrosis factor-alpha (TNF-ot) and interleukin-6 (IL-6) contents (by ELISA) , and phosphor-signal transducer and activator of transcription 1 (p-STAT1) expression (by Western blot), and for examination of the pathological changes (with light microscope).Results Compared with S group , the CK-MB activity and cTnI concentration in serum and contents of TNF-α and IL-6 were significantly increased, and the expression of p-STAT1 was up-regulated in HS/R and Sev groups (P＜0.05).Compared with HS/R group, the CK-MB activity and cTnI concentration in serum and contents of TNF-α and IL-6 were significantly decreased, and the expression of p-STAT1 was downregulated (P＜0.05) , and the pathological changes of myocardia were alleviated in Sev group.Conclusion Sevoflurane can alleviate HS/R-induced damage to myocardia of pigs, and inhibited STAT1 activity and attenuated inflammatory responses in the myocardium are involved in the mechanism.

Objective To evaluate the changes in the expression of aquaporin-8 (AQP8) in intestinal mucosa in pigs with hemorrhagic shock.Methods Sixteen Bama miniature pigs,weighing 22-25 kg,were equally and randomly divided into sham operation group (group S) and hemorrhagic shock group (group HS).The animals were fasted for 8 h before operation.The animals were anesthetized with propofol 3 mg/kg injected via the auricular vein,and tracheostomized and mechanically ventilated.In group S,the femoral artery and internal jugular vein were only cannulated.In group HS,the femoral artery and internal jugular vein were cannulated for blood pressure and mean arterial pressure monitoring and blood sampling.Hemorrhagic shock was then induced by removing 40 percent of blood volume over 15 min.Before anesthesia (T0),and at 30 min and 1.0,1.5,2.0,3.0 and 4.0 h after the end of blood-letting (T1.6),blood samples were collected for determination of serum D-lactate and intestinal fatty acid binding protein (I-FABP) concentrations.After blood sampling at T6,the pigs were sacrificed,and intestinal specimens were obtained for microscopic examination and for determination of AQP8 cotent in intestinal mucosa (by ELISA).The water content of intestines was calculated by wet/dry weight ratio.Results Compared with group S,the serum D-lactate concentrations at T2-6,I-FABP concentrations at T1-6,and water content of intestines were significantly increased,and the cotent of AQP8 was up-regulated at T6 in group HS.No changes were found in the intestinal mucosa in group S.In group HS,severe damage to the intestinal mucosa was found,and bleeding,inflammatory cell infiltration,and epithelial cell necrosis were observed.Conclusion The mechanism of hemorrhagic shock-caused damage to intestines is related to up-regulated expression of AQP8 in intestinal mucosa in pigs.

Objective To evaluate the effect of sevoflurane on brain injury in pigs with hemorrhagic shock (HS).Methods Twenty-four adult male Bama miniature pigs, aged 6 months, weighing 22-25 kg, were equally and randomly divided into 3 groups using a random number table: sham operation group (group Sham) , group HS, and sevoflurane group (S group).In group Sham, the bilateral femoral arteries and internal jugular vein were only punctured.The animals were anesthetized with iv propofol 3.0 mg/kg, tracheostomized and mechanically ventilated.The right femoral artery was cannulated for blood-letting.HS was induced by blood-letting (40％ blood volume within 15 min), and it was then maintained for 1 h after the end of blood-letting to induce brain injury.In group S, 2％ sevoflurane was inhaled for 30 min after successful establishment of the model.Immediately before establishment of the model (T0) , and at 30, 60,90, 120, 180 and 240 min after HS (T1-6) , blood samples were collected from the internal jugular vein for determination of interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) concentrations in serum (by enzyme-linked immunosorbent assay), and neuron-specific enolase (NSE) and S-100β protein concentrations in serum (using double antibody sandwich method).Results Compared with group Sham, the serum IL-1β, TNF-α, NSE and S-100β protein concentrations were significantly increased at T2-6 in HS and S groups (P＜0.05).Compared with group HS, the serum IL-1β, TNF-α, NSE and S-100β protein concentrations were significantly decreased at T3-6 in group S (P＜ 0.05).Conclusion Sevoflurane can mitigate brain injury in pigs with HS, and the mechanism is associated with inhibition of inflammatory responses.