Objective To provide new experimental evidences associated with the mechanisms of inhaled anesthetics, the effects of sevoflurane on the electric activities of inhibitory interneurons in basal forebrain area (BF) were observed.Methods C57BL/6 mice, aged 2-3 weeks, were used and BF sections were cut for whole patch-clamp recording.Artificial cerebrospinal fluid containing sevoflurane was given and action potential, inhibitory postsynaptic potential were recorded.Results Sevoflurane could increase the frequency of firing rate of inhibitory interneurons in basal forebrain area (P<0.001), which could increase the frequency of action potential caused by depolarization current (P<0.05), and increase the frequency of spontaneous inhibitory postsynaptic currents of pyramidal neurons (P<0.05), while AP-depended miniature inhibitory postsynaptic currents were not significantly changed.Conclusion The basal forebrain inhibitory interneurons are involved in the anesthetic effect of sevoflurane.

Objective To evaluate the effect of sevoflurane preconditioning on the function of sar-coplasmic reticulum in cardiomyocytes during ischemia-reperfusion (I∕R) in isolated rat hearts. Methods Healthy adult male Sprague-Dawley rats, weighing 270-300 g, were anesthetized with intraperitoneal pen-tobarbital. Their hearts were excised and perfused in a Langendorff apparatus with K-H solution saturated with 95％ O2-5％ CO2 at 37 ℃ . Twenty-four isolated rat hearts successfully perfused in the Langendorff ap-paratus were divided into 3 groups (n= 8 each) using a random number table: control group (group C), I∕R group and sevoflurane preconditioning group (group SP). Myocardial ischemia was induced by interrup-ting perfusion for 30 min followed by 120 min reperfusion. In group SP, the hearts were perfused with 2. 4％ sevoflurane for 10 min starting from 10 min before ischemia. Left ventricular developed pressure (LVDP) and left ventricular end-diastolic pressure (LVEDP) were recorded at 5, 10, 15, 30 and 60 min of reperfusion. Coronary effluent was collected at 10 min before reperfusion for measurement of the levels of lactate dehydrogenase (LDH) and cardiac troponin I (cTnI). Myocardial specimens were obtained at 120 min of reperfusion for examination of the pathological changes (using HE staining) and for determination of myocardial infarct size (by TTC staining), sarcoendoplasmic reticulum Ca2+-ATPase (SERCA2a) activity (with a spectrophotometer) and expression of Bcl-2, Bax and SERCA2a ( by Western blot). Results Compared with group C, LVDP was significantly decreased and LVEDP was increased at each time point, myocardial infarct size was increased, the levels of LDH and cTnI in coronary effluent were increased, the expression of Bax was up-regulated, the expression of Bcl-2 and SERCA2a was down-regulated, and the activity of SERCA2a was decreased in group I∕R (P<0. 01). Compared with group I∕R, LVDP was signifi-cantly increased and LVEDP was decreased at each time point, myocardial infarct size was decreased, the levels of LDH and cTnI in coronary effluent were decreased, the expression of Bax was down-regulated, the expression of Bcl-2 and SERCA2a was up-regulated, the activity of SERCA2a was increased (P<0. 01), and the pathological changes were significantly attenuated in group SP. Conclusion The mechanism by which sevoflurane preconditioning reduces I∕R injury in isolated rat hearts may be related to improving the function of sarcoplasmic reticulum in cardiomyocytes.