摘要
目的:探讨四氢巴马汀(l-THP)对大鼠心肌缺血再灌注损伤的保护作用。方法:Wistar大鼠24只,分为假手术组、模型组和l-THP治疗组,结扎大鼠冠状动脉左前降支30min再灌注120min造成心肌缺血再灌注损伤模型,分别于缺血30min、再灌注30min、60min、90min、120min观察l-THP对大鼠心功能、心肌酶学和脂质过氧化的影响。结果:l-THP能够对抗心肌缺血再灌注损伤引起的左心室内压(LVSP)、左心室内压最大上升与下降速率(±dp/dtmax)下降,左心室舒张末期压力(LVEDP)的升高,并能够稳定心肌组织Na+-K+-ATPase和Ca2+-Mg2+-ATPase活性,降低丙二醛(MDA)含量和增高超氧化物歧化酶(SOD)的活性。结论:四氢巴马汀(l-THP)对大鼠心肌缺血再灌注引起的心功能降低具有明显的保护作用,其机制可能与改善能量代谢障碍和抑制自由基生成或清除氧自由基作用有关。
Objective:To investigate the protective effects of l-tetrahydropalmatine(l-THP) on the cardiac function in rats suffered from myocardial ischemic reperfusion injury in rats.Methods:Twenty four healthy Wistar rats weighing 230±25 g were randomly divided into 3 groups(n=8 each),sham operation group;ischemic reperfusion group(I/R);l-THP+ I/R group.Myocardial ischemic reperfusion injury model was established by the ligation of left anterior descending coronary artery for 30 min and referfusion for 120 min in rats.In myocardial ischemia 30 min,reperfusion 30 min,60 min,90 min,120 min, the influence of l-THP on the cardiac function,myocardial enzymes and lipid peroxide of myocardium were observed.Results:l-THP attenuated declines of the amplitudes of LVSP and±dp/dtmax,and attenuated the increasing of LVEDP.l-THP increased Na+-K+-ATPase and Ca2+-Mg2+-ATPase activity, decreased level of malondialdehyde(MDA) production and increased superoxide dismutase(SOD) actitvity in the ischemic myocardium.Conclusion:The effects of l-THP alleviating injury on cardiac function in the process of ischemic reperfusion may be related to the mechanism of improving energy metabolism,scavenging the oxygen free radicals and inhibiting production of free.
出处
《中国误诊学杂志》
CAS
2007年第23期5462-5465,共4页
Chinese Journal of Misdiagnostics
基金
咸宁学院院基金资助重点项目(编号:XY9903)