右美托咪定预处理对大鼠心肌缺血再灌注损伤产生氧化应激的影响

Effects of Dexmedetomidine Preconditioning on Oxidative Stress Induced by Myocardial Ischemia-reperfusion Injury in Rats

目的:探讨右美托咪定对大鼠心肌缺血再灌注损伤产生氧化应激的影响方法:选取SD雄性大鼠45只,随机分为三组:假手术组(S组);心肌缺血-再灌注组(IR组);右美托咪定预处理+IR组(IRD组),每组15只。三组大鼠麻醉后分离右股静脉并置管,右美托咪定组在缺血前30 min给予右美托咪定,其余组在同一时间经股静脉给予等量生理盐水。分别记录缺血前(TO)、结扎30 min(T1)、再灌注1 h(T2)和再灌注2 h(T3)时的HR、左室内压最大上升速率(+dp/dtmax)和左室内压最大下降速率(-dp/dtmax)和左室舒张末压(LVEDP),比较3组大鼠血中超氧化物歧化酶(SOD)、心肌肌钙蛋白I(cTnI)水平。结果:右美托咪定预处理能够缓解大鼠心肌缺血再灌注损伤产生的氧化应激。

Objective: To investigate the effect of dexmedetomidine on oxidative stress induced by myocardial ischemia reperfusion injury in rats.Methods: Forty-five SD male rats were randomly divided into three groups: sham operation group(S group);myocardial ischemia-reperfusion group(IR group);dexmedetomidine pretreatment + IR group(IRD group). 15 in each group. The rats in the three groups were anesthetized and the right femoral vein was separated and placed in the tube. The dexmedetomidine group was given dexmedetomidine 30 min before ischemia. The other groups were given the same amount of normal saline through the femoral vein at the same time.HR, left ventricular maximum pressure(+dp/dtmax) and left ventricular maximum pressure were recorded before ischemia(TO), ligation for 30 min(T1), reperfusion for 1 h(T2), and reperfusion for 2 h(T3). Rate(-dp/dtmax) and left ventricular end-diastolic pressure(LVEDP) were compared. The levels of superoxide dismutase(SOD) and cardiac troponin I(cTnI) in the blood of the three groups were compared. RESULTS: Prednitomidine preconditioning attenuated oxidative stress induced by myocardial ischemia-reperfusion injury in rats.