The effects of diazoxide on myocardium function and the expressions of ERK and JNK in isolated spontaneous hypertension rat hearts / 中国应用生理学杂志

<p><b>AIM</b>To investigate the effect of diazoxide preconditioning and the role of ERK and JNK in cellular signaling during diazoxide preconditioning protection in isolated spontaneous hypertension rat (SHR) hearts.</p><p><b>METHODS</b>Hearts were isolated from male SHR rats, and perfused on a Langendorff apparatus. Five groups were considered (n = 6). Con: after 40 min perfusion the hearts were submitted to 25 min ischemia followed by 30 min reperfusion. IP: the hearts were preconditioned with 2 periods of 5 min ischemia and 10 min reperfusion prior to 25 min ischemia. DP: the hearts were preconditioned with 2 periods of 10 min K-H solution with 50 micromol x L(-1) diazoxide and 5 min K-H solution reperfusion prior to 25 min ischemia. 5-HD: perfuse with 100 micromol x L(-1) 5-HD (a special mitochondrial ATP sensitive potassium channel blocker) for 10 min followed by 30 min K-H solution perfusion before 25 min ischemia. 5-HD + DP: 100 micromol x L(-1) 5-HD was given for 10 min before diazoxide preconditioning.</p><p><b>RESULTS</b>During reperfusion, comparing with Con group, the recoveries of left ventricle developed pressure (LVDP), + dP/dt(max), - dP/dt(max) and left ventricle end diastolic pressure (LVEDP) were improved in IP and DP groups (P < 0.01 vs Con). At the end of reperfusion, compared with Con group, the expression of ERK in myocardium were higher in IP and DP groups (P < 0.01 vs Con), there was no significance between 5-HD and Con group, but 5-HD couldn't inhibit the expression of ERK induced by diazoxide preconditioning. The expression of JNK in IP and DP groups were decreased (P < 0.05 vs Con), this effect could been inhibited by 5-HD.</p><p><b>CONCLUSION</b>These results indicated that diazoxide preconditioning could mimic ischemic preconditioning, the activation of ERK expression and the declining of JNK expression involved in diazoxide preconditioning in isolated SHR hearts.</p>

Effects of lidocaine and thiopental on the neuronal injury in rat hippocampus slice cultures / 中国应用生理学杂志

<p><b>AIM</b>To observe the effects of lidocaine and thiopental on the neuronal injury induced by the experimental ischemia in hippocampus slice cultures obtained from postnatal 22 days SD rats.</p><p><b>METHODS</b>Model of the experimental ischemia was produced by hypoxia and glucose deprivation. Propidium iodide (PI) assay was used to observe the neuronal injury in CA1 and dentate gyrus (DG).</p><p><b>RESULTS</b>After experimental ischemia, the peak of PI index was appeared in CA1 and DG on the first day (P < 0.01), PI index in DG was less than in CA1 (P < 0.01). PI indices were still higher during seven days after the experimental ischemia than before the experimental ischemia (P < 0.01). 10 nmol/L and 100 nmol/L concentration of lidocaine could significantly decrease PI indices in CA1 and DG (P < 0.01). 250 nmol/L and 600 nmol/L concentration of thiopental also decreased the PI indices in CA1 and DG (P < 0.01). The neuronal injury peaks were postponed to the third day after the experimental ischemia by lidocaine and thiopental.</p><p><b>CONCLUSION</b>It suggested that lidocaine and thiopental could decrease the neuronal injury in CA1 and DG induced by the experimental ischemia, and postpone the neuronal injury peaks to the third day after the experimental ischemia.</p>

Propofol depresses c -fos expression of NOS neurons in the spinal cord of rats with inflammatory pain / 生理学报

In formalin pain model, the effect of propofol on Fos expression in the spinal cord was examined by means of c -fos oncogene immunohistochemistry and NADPH-d histochemistry. Fos-like immunoreactive (FLI) neurons were mainly found in the ipsilateral dorsal horn after injection of formalin, some of which were FLI/NOS double-labeled neurons. Most of the FLI or FLI/NOS double-labeled neurons were observed in the medial part of lamina and the outer lamina . Before or after injection of formain, i.p. injection of propofol significantly decreased the number of FLI and FLI/NOS double-labeled neurons in all laminae (P<0.05 or P<0.01). By single i.p. injection of propofol or normal saline, few FLI neurons were found in the spinal cord. The results suggest that the antinociceptive function of propofol is possibly involved in the depression of the NOS neurons in the spinal cord.

Effect of medial preoptic area destruction on the anesthesia induced with propofol and ketamine / 中华麻醉学杂志

Objective To investigate the effect of medial preoptic area ( mPOA) destruction on the anesthesia induced with propofol and ketamine and the role of mPOA in the mechanism of anesthesia. Methods Twenty-four SD rats weighing 250-300 g were randomly divided into two groups: NS group ( n = 12) and NMDA destruction group ( n = 12) . The animals were anesthetized with intraperitoneal (ip) pentobarbital 40 mg?kg-1. A hole was drilled in the skull fixed by a stereotactic apparatus (Narishige). 0.5?l of normal saline (NS) or N-methyl-D-aspartate (NMDA) was injected into mPOA. The rats were observed for changes in behaviour and body weight. On the 7 th day after NS or NMDA injection each group was further divided into 2 subgroups receiving either propofol 100 mg?kg-1 or ketamine 100 mg?kg-1 ip. The latency of loss of righting reflex (RL)(time from end of ip injection to loss of righting reflex) and recovery time (RT) were recorded. Results There were no significant changes in behaviour and body weight after mPOA injection in NS group; while animals in NMDA-destruction group showed increased excitability , irritability and activity and decreased appetite and sleep and significant weight loss after mPOA injection. RL was significantly longer and RT was significantly shorter after propofol/ketamine ip injection in NMDA destruction group than those in NS group. Conclusion mPOA is probably involved in anesthesia induced with propofol and ketamine.