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 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 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 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 efficiency of transduction of recombinant adenovirus-mediated human endothelial nitric oxide synthase (eNOS) into lung tissue by repeated intratracheal transfection in rats.Methods Sixty 3-4 month old male Wistar rats weighing 220-280 g were randomly divided into 2 groups:control group (group C,n =10) and eNOS gene transduction group (group T,n =50).The animals were anesthetized with intraperitoneal 10％ chloral hydrate 35 mg/kg,tracheally intubated and mechanically ventilated (VT 2.5 ml,RR 60 bpm,FiO2 1.0).Recombinant adenovirus carrying human eNOS gene was given as gift by Professor Gerard from Texas University,Southwest Medical Center.In group T 50 μl of the recombinant adenovirus in concentration of 5 × 109 PFU/ml was instilled into trachea every 5 minutes for 12 times,while in group C equal volume of vector conservation solution was instilled instead.Pulmonary arterial blood samples were obtained at 2,5,7,14 and 21 d after intratracheal transfection (n =10 at each time point) for determination of serum NO concentration.The animals were immediately sacrificed after blood sample collection for determination of expression of eNOS protein in the lung tissue and RNA.The eNOS expression in the trachea,bronchus,lung,liver,spleen and kidney was detected by immuno-histochemistry.Results The serum NO concentrations were significantly higher at all time points in group T than in group C.The eNOS expression was detected in the epithelial cells of trachea and bronchi,and endothelial cells of alveoli and pulmonary blood vessels in group T but not in group C.eNOS expression was not detected in liver,spleen and kidney at 7 d after intratracheal transfection in group T.Conclusion Human eNOS gene mediated by recombinant adenovirus was transducted into rat lung tissue with normal enzyme activity by repeated intratracheal administration without being detected in distant organs.

Clinical, radiological and pathological presentations in two children with epidermal nevus syndrome were analyzed and relevant literature was reviewed.Two patients both had typical epidermal nevus and abnormal cerebral radiography, which was associated with mental retardation, epilepsy, language and movement retardation.One case was complicated with an ocular tumor.Pathological investigations of the epidermal nevus revealed papilliform proliferation in squamous epidermis.The disorder may have a systemic involvement besides cutaneous lesions, with a predilection for the central nervous system.Early diagnosis and therapy may help to improve patients life quality.

Objective To investigate the effect of monosialoganglioside GM-1 on cardiopulmonary bypass (CPB)-induced brain injury in rats.Methods Twenty-seven adult male Sprague-Dawley rats,weighing 350-450 g,aged 15 months,were randomly divided into 3 groups (n=9 each): control group (C group),CPB group and GM-1 group.The animals were anesthetized with chloral hydrate,tracheostomized and mechanically ventilated.Right common carotid and right jugular vein were cannulated for closed-chest CPB.In groups CPB and GM-1,the rats underwent 1 h CPB.GM-1 20 mg/kg was added to the priming solution in group GM-1,while the equal volume of normal saline was given in group CPB.The animals were sacrificed at 3 h after termination of CPB or 3 h after the end of ventilation in group C,the brains were removed and the hippocampi isolated for microscopic examination and for determination of apoptosis (using TUNEL) and Bax and Bcl-2 protein expression (by immunohistochemistry and Western blot).Results Compared with group C,the number of apoptotic neurons and ratio of Bax/Bcl-2 were significantly increased,and the expression of Bcl-2 and Bax protein was up-regulated in groups CPB and GM-1 (P ＜ 0.05).Compared with group CPB,the number of apoptotic neurons and ratio of Bax/Bcl-2 were significantly decreased,the expression of Bax protein was down-regulated and the expression of Bcl-2 protein was up-regulated in group GM-1.The pathological changes were severe in group CPB and attenuated in group GM-1.Conclusion GM-1 can attenuate CPB-induced brain injury in rats and inhibition of the apoptosis in neurons may be involved in the mechanism.

Objective To evaluate the effect of sevoflurane on activation of nuclear factor kappa B (NF-κB) during brain injury induced by hemorrhagic shock (HS) in pigs.Methods Thirty-two adult male Bama miniature pigs,aged 6 months,weighing 22-25 kg,were divided into 4 groups (n=8 each) using a random number table:sham operation group (group Sham),HS group,sevoflurane preconditioning group (group Sev-Pre) and sevoflurane postconditioning group (group Sev-Post).The animals were anesthetized,and tracheostomized and mechanically ventilated.In group Sham,the bilateral femoral arteries and internal jugular veins were only cannulated.HS was induced by removing 40％ of blood volume within 15 min (30 ml/kg) via the right femoral artery and maintaining at this level for 1 h before resuscitation in HS,Sev-Pre and Sev-Post groups.In group Sev-Pre,2％ sevoflurane was inhaled for 30 min,and then HS was induced.In group Sev-Post,2％ sevoflurane was inhaled for 30 min starting from the time point immediately after HS was induced.Immediately before establishment of the model and at 30,60,90,120,180 and 240 min of HS (T1-6),blood samples from the jugular vein were collected for determination of serum interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) concentrations by enzymelinked immunosorbent assay.At 4 h of HS,the rats were sacrificed,and brains were removed for microscopic examination of hippocampal CA1 region (using haematoxylin and eosin staining) and for determination of the expression of NF-κB in nucleoprotein (by Western blot).Results Compared with group Sham,the concentrations of serum IL-1β and TNF-α were significantly increased at T2-6,and the expression of NF-κB in nucleoprotein in hippocampal CA1 region was up-regulated in HS,Sev-Pre and Sev-Post groups (P＜0.05).Compared with group HS,the concentrations of serum IL-1β and TNF-α were significantly decreased at T3-6,and the expression of NF-κB in nucleoprotein in hippocampal CA1 region was down-regulated in Sev-Pre and Sev-Post groups (P＜0.05).There were no significant differences between group SevPre and group Sev-Post in concentrations of serum IL-1β and TNF-α and expression of NF-κB in nucleoprotein in hippocampal CA1 region (P＞0.05).The pathologic changes were significantly attenuated in SevPre and Sev-Post groups as compared with group HS.Conclusion The mechanism by which sevoflurane attenuates brain injury induced by HS may be related to inhibition of NF-κB activation and reduction of inflammatory responses in pigs.