RESUMO
Objective To investigate the effect of sevoflurane preconditioning on CCAAT/enhancer binding protein (C/EBP) homologous protein (CHOP) expression in the cerebral cortex after focal cerebral ischemiareperfusion (I/R) injury in rats and the mechanism. Methods Thirty-six male SD rats weighing 250-280 g were randomly divided into 3 groups ( n = 12 each) : sham operation group (group S) , focal cerebral I/R group (group I/R) and sevoflurane preconditioning group (group Sevo-pc). The animals were anesthetized with intraperitoneal chloral hydrate 300 mg/kg. In groups I/R and Sevo-pc, focal cerebral ischemia was induced by middle cerebral artery occlusion using a nylon thread with rounded tip inserted into the right internal carotid artery and advanced cranially until resistance was met. The occlusion was maintained for 1 h followed by 24 h reperfusion. Group Sevo-pc inhaled 2.7% sevoflurane for 1 h before ischemia. Neurological deficits were assessed and scored at the end of 24 h reperfusion and then the rats were decapitated. Their brains were immediately removed. The cerebral infarct size was determined by TTC staining. The CHOP expression in the ischemic cerebral cortex was determined by immunohistochemistry. The number of apoptotic neurons was counted using TUNEL. Results The neurological deficit scores were significantly higher, the cerebral infarct size was significantly larger, and the CHOP expression and the number of apoptotic neurons were significantly higher in groups I/R and Sevo-pc than in group S ( P ＜ 0.01) . The neurological deficit scores were significantly lower, the cerebral infarct size was significantly smaller, and the CHOP expression and the number of apoptosis neurons were significantly lower in group Sevo-pc than in group I/R ( P ＜ 0.05 or 0.01) . Conclusion Sevoflurane preconditioning may protect the brain against focal cerebral I/R injury by down-regulating CHOP expression in the cerebral cortex in rats.
RESUMO
Objective To evaluate the myocardial protective effect of pretreatment with pinacidil, a potassium channel opener, on myocardium perfused intermittently with normothermic or hypothermic high potassium crystalloid cardioplegie solution during cardiopulmonary bypass ( CPB) . Methods Eighteen dogs of both sexes weighing 10-15 kg were intubated and mechanically ventilated after induction of anesthesia. Femoral artery and vein were cannulated for direct MAP and CVP monitoring. Swan-ganz catheter was placed via right internal jugular vein. The animals were randomly divided into 3 groups: group A (hypothermic CPB) in which heart was perfused with 4℃ St Thomas solution 10 ml?kg-1 in 2 min and 30 min later perfused again with half of the initial volume(5 ml? kg-1); in group B (normotherinic CPB) and group C (hypothermic CPB) heart was pretreated with oxygenated pinacidil solution (0.083 mg?kg-1 37℃) before cardioplegia. The heart was subjected to 60 min global ischemia followed by 30 min reperfusion. The hemodynamic changes were measured before aortic cross-clamping and 15 and 30 min after release of aortic cross-clamping. Myocardial tissue was obtained from apex of left ventricle for determination of myocardial adenine nucleotide content 5 min after CPB was initiated, 30 and 60 min after aortic cross-clamping and 20 min after reperfusion. Results During reperfusion the hemodynamic function and myocardial ATP content recovered significantly better in group C than those in group A and B ( P