组织源性血管紧张素Ⅱ介导大鼠心肌缺血预处理

Ischemic Preconditioning Mediated by Tissue derived Angiotensin Ⅱ in Rat Heart

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摘要目的：探讨组织源性血管紧张素Ⅱ（ＡｎｇⅡ）在大鼠心肌缺血预处理中的作用。方法：采用Ｌａｎｇｅｎｄｏｒｆ灌流技术，以停灌注４５分钟、再灌注１５分钟造成缺血再灌注损伤模型，观察缺血预处理对缺血再灌注损伤心肌的保护作用，及洛沙坦（ｌｏｓａｒｔａｎ）对这一作用的影响。采用放射免疫法测定心肌组织ＡｎｇⅡ含量。结果：缺血再灌注后，冠状动脉流出液中肌酸激酶、乳酸脱氢酶和肌红蛋白分别较对照组升高１７倍、１２倍和１１倍（Ｐ＜０．０１），组织丙二醛和钙含量分别增加５倍和１倍（Ｐ＜０．０１），缺血预处理使这些变化得到明显改善，而预处理前给予１０－６ｍｏｌ／Ｌ洛沙坦，则预处理的保护作用消失，组织ＡｎｇⅡ的变化与上述指标的变化相平行。还发现，５分钟停灌注反复３次后，组织ＡｎｇⅡ明显高于对照组（Ｐ＜０．０５），而又显著低于缺血再灌注组（Ｐ＜０．０１）。结论：在缺血预处理对缺血再灌注损伤心肌的保护作用中，ＡｎｇⅡ是介导心肌缺血预处理的主要介质之一。 Objective:To study the effect of tissue derived angiotensin Ⅱ on ischemic preconditioning in rats. Methods:Using Langendorff perfusion technique,the ischemia reperfusion injury model was established by ceasing perfusion for 45 minutes,and reperfusion for 15 minutes.The protective effect of ischemic preconditioning and the influence of losartan was observed. Results:After ceasing perfusion for 45 minutes and reperfusion for 15 minutes,the CK,LDH and myoglobin in coronary artery effusion increased 17 fold,12 fold and 11 fold,while tissue MDA and calcium increased 5 fold and 1 fold,respectively,as compared with control group( p <0 01).Ischemic preconditioning markedly reversed the above changes but the above protective effect disappeared by adding 10 6 mol/L losartan before ischemic preconditioning.The change of tissue angiotensin Ⅱ is parallel to the changes of the above indices.Simply by ceasing perfusion 5 minutes for 3 times,we found tissue angiotensin Ⅱ was significantly higher than control( p <0 05),but lower than ischemia reperfusion group( p <0 01). Conclusion:Ischemic preconditioning can obviously protect ischemic reperfusion injured myocardium.Angiotensin Ⅱ is one of the main mediators of ischemic preconditioning.