摘要
目的:探讨地塞米松预处理对缺血再灌注大鼠血流动力学和心肌超微结构的影响。方法:将SD大鼠予地塞米松预处理,生理盐水预处理设为对照。预处理24 h后构建Langendorff离体心脏缺血再灌注动物模型,动态观测缺血前及再灌注期间血流动力学的改变;观察大鼠心肌超微结构及热休克蛋白72(HSP72)表达变化。结果:地塞米松预处理诱导大鼠心肌HSP72的表达较对照组显著增加(P<0.05);地塞米松可改善再灌注期间血流动力学指标(左心室发展压、左心室收缩的最大速率、左心室舒张的最大速率、冠状动脉循环流出量,P<0.01)及减轻缺血再灌注后心肌超微结构的损伤。结论:地塞米松预处理对缺血再灌注大鼠的心脏具有延迟保护作用。
Objective： To explore the effects of dexamethasone （DEX） on hemodynamics and myocardial ultrastructure in rats during ischemia/reperfusion. Methods： The rats were pretreated with DEX in 24 hours before their hearts were separated for Langendorff perfusion and for ischemia/reperfusion. Rats in control group were pretreated with sodium chloride. The left ventricular functions （LVDP, ＋ dp/dtmax, -dp/dtmax） and coronary artery flow （CF） were observed dynamically before ischemia and during 60-minute reperfusion following 30-minute ischemia. Myocardial ultrastructures were also examined. Heat shock protein 72 （HSP72） expression was checked by using immunohistochemistry technique. Results： Compared with control group,in DEX pretreated rats, the expression of HSP72 was significantly increased （P 〈 0.05 ）, the LVDP, ＋ dp/dtmax, - dp/dtmax and CF were greatly improved （P 〈0.01 ）, and the creased. Conclusions： DEX induces u ischemia/reperfusion injury of myocardial ultrastructure was depregulation of HSP72, which functions to protect myocardium against ischemia/reperfusion injury in rat heart.
出处
《贵阳医学院学报》
CAS
2007年第1期24-28,共5页
Journal of Guiyang Medical College
