Objective To evaluate the effect of hypothermia on the pharmacokinetics of rocuronium in the pigs with hemorrhagic shock.Methods Thirty-two Bama mini pigs of both sexes,aged 4-6 months,weighing 22-25 kg,were randomly divided into 4 groups (n=8 each) using a random number table:normal temperature control group (group NC),normal temperature+hemorrhagic shock group (group NH),hypothermia control group (group HC),and hypothermia+hemorrhagic shock group (group HH).NC and NH groups were put in the normal temperature environment,and HC and HH groups were put in a freezer at-15 ℃.In NC and HC groups,rocuronium 3.78 mg/kg was injected via the auricular vein after the animals were awake.In NH and HH groups,hemorrhagic shock was then induced by removing 40％ of blood volume from the right femoral artery at a constant speed within 15 min (30 ml/kg),and rocuronium 3.78 mg/kg was injected via the auricular vein at 30 min after the model was successfully established.At 0 (T0),2 (T1),4 (T2),7 (T3),10 (T4),15 (T5),20 (T6),30 (T7),60 (T8),120 (T9),180 (T10),240 (T11) and 300 min (T12) after rocuronium injection,blood samples were collected from the internal jugular vein for determination of the blood concentration of rocuronium by high performance liquid chromatography-tandem mass spectrometry method.The maximum concentration (Cmax),elimination half-life (t1/2),plasma effect-site equilibration rate content (Ke0),area under concentration curve,and mean residence time (MRT) of rocuronium were calculated.Results Compared with group NC,the blood concentration of rocuronium was significantly decreased at T5-T12 in group NH,the blood concentration of rocuronium was significantly increased at T5-T12 in group HC,and t1/2 was significantly prolonged,Ke0 was decreased,and MRT was prolonged in NH and HC groups (P＜0.05 or 0.01).Compared with group HC,the blood concentration of rocuronium was significantly increased at T4-T12,t1/2 was prolonged,Ke0 was decreased,and MRT was prolonged in group HH (P＜0.05).Compared with group NH,the blood concentration of rocuronium was significantly increased at T5-T11,t1/2 was prolonged,Ke0 was decreased,and MRT was prolonged in group HH (P＜ 0.05).Conclusion Hypothermia can reduce the pharmacokinetics of rocuronium in the pigs with hemorrhagic shock.

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 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 investigate the protective effects of propofol on liver against hypoxia/reoxgenation (H/R) injury in rats. Methods Twenty-four Wistar rats of both sexet weighing 200-250g were randomized into control group (group A), hypoxia/reoxygenation group (group B) and H/R + propofol group (group C). The 8-iso-prostaglandin F 2? (8-iso-PGF 2? ) level in the hepatic tissue was determined by enzyme-linked immunosorbent assay (ELISA). The content of NO and the activity of NOS were assessed by biochemical methods. Results In group B, the 8-iso-PGF 2? level in hepatic tissue was significantly higher than that in group A (P

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

Objective To investigate the preventive effects of midazolam and propofol on liver against hypoxia/reoxgenation(H/R) injury in rats.Methods Twenty-four Wistar rats of both sexes weighing 200-250g were randomized into four groups:control group(group A),hypoxia/reoxygenation(group B),H/R + midazolam(group C) and H/R + propofol(group D).The 8-iso-prostaglandin F2?(8-iso-PGF2?) levels in the hepatic tissue were determined by enzyme-linked immunosorbent assay(ELISA).The contents of nitric oxide(NO) and the activity of nitric-oxide synthase(NOS) in hepatic tissue were determined by biochemistry methods.Results After hypoxia and reoxgenation injury in rats,the 8-iso-PGF2? level of hepatic tissue in group B was significantly higher than that in group A(P

Objective To investigate the effect of propofol on C-fos expression and glutamate concentration in rat cerebral cortex induced by ketamine. Methods Twenty-eight male Wistar rats weighing 260-280 g were randomly divided into four groups of seven animals: group 1 received normal saline intraperitoneally (ip) (group NS); group 2 received NS + ketamine 100mg?kg-1 ip (group K); group 3 received propofol 100 mg?kg-1 + ketamine 100mg?kg-1 ip (group PK); group 4 received diazepam 10mg?kg-1 + ketamine 100 mg?kg-1 ip (group DK). The interval between the two intraperitoneal injections was 5 min in each group. The animals were decapitated 30 min after ip injection. C-fos mRNA expression was detected by RT-PCR method and fos protein expression by immuno-histochemical technique. Another forty Wistar rats were randomly divided into 4 groups of 10 animals as was described above. Two hours after ip injection, five animals in each group were decapitated for microscopic examination and the other five animals for determination of water and glutamate content of cerebral cortex.Results C-fos mRNA expression increased at 30 min after intraperitoneal ketamine. Ketamine induced significant increase in Fos protein expression, and glutamate and water content in cerebral cortex 2 h after ip injection. Propofol and diazepam inhibited the increases induced by ketamine ( P

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

The aim of this study was to investigate the effects of nifedipine on stress responses to tracheal intubation. Thirty adult patients, ASA Ⅰ to Ⅱ, scheduled for elective surgery, were randomly assigned to receiving intravenous infusion of normal saline 30ml (group Ⅰ). fentanyl 5?g/kg (group Ⅱ) or nifedipine 40 ?g/kg(group Ⅲ), respectively. After intravenous thiopental, valium and atracurium. the tracheal intubation was performed. SP, DP, HR and RPP were determined before administration, immediately before and after intubation. 1, 3 and 5 min following intubation separately, and the venous blood samples were taken at correspondingly later 5 times to measure plasma concentrations of endotheline(EF), atrial natriuretic polypeptide (ANP), TXB_2 and 6-keto-PGF_1 ? by radioimmunoassay individually. Following intubation. MAP went up in group Ⅰ and transiently in group Ⅱ and Ⅲ, HR in creased by 36.6% and 33.3% in group Ⅰ and Ⅲ and remained stable in group Ⅱ, RPP rose in group Ⅰ and rept statistically unchanged in group Ⅱ and Ⅲ, ET level stayed constant in all three groups, levels of ANP and TXB_2 ascended in group Ⅰ, transiently in group Ⅱ and did not vary in group Ⅲ, 6-keto-PGF_1? level were raised in group Ⅱ, transiently in group Ⅲ and did not change in group Ⅰ, and TXB_2/6-keto-PGF_1? ratio(T/K) shoot up in group Ⅰ and reduced in group Ⅱ and Ⅲ. As compared with those in group Ⅰ, before intubation, ANP level increased in group Ⅱ and Ⅲ. 6-keto-PGF_1? level decreased and T/K rose in group Ⅲ; after intubation, levels of ANP and 6-keto-PGF_1 ? went up in group F, transiently in group Ⅲ, and TXB_2 and T/K values went down in group Ⅱ and Ⅲ. It is suggested that prophylactic intravenous nifedipine may effectively depress the cardiovascular and hormone responses to tracheal intubation, but can not take complete place of fentanyl for this procedure.