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目的:观察西拉普利和阿司匹林对实验性大鼠心肌梗死(MI)后心脏间质胶原代谢的影响。方法:采用结扎冠状动脉(冠脉)左前降支的方法建立大鼠MI模型,设立假手术组、梗死组、西拉普利组、阿司匹林组、联合组。术后2周测定循环中血管紧张素Ⅱ(AngⅡ)、6酮PGF1α(6ketoPGF1α)、内皮素1(ET1)水平和心脏梗死区、左室非梗死区及右室的间质胶原含量。结果:各实验组与假手术组比较,血循环中AngⅡ、ET1升高,6ketoPGF1α降低,左室非梗死区及右室的胶原含量明显升高。各实验组间梗死区的胶原含量相互比较差异无统计学意义。与梗死组比较,阿司匹林组血6ketoPGF1α显著降低,左室非梗死区及右室的胶原含量差异无统计学意义;西拉普利组、联合组血AngⅡ、ET1明显降低,6ketoPGF1α显著升高,左室非梗死区及右室的胶原含量明显降低。联合组与西拉普利组比较,6ketoPGF1α显著降低,而左室非梗死区及右室的胶原含量差异无统计学意义。结论:MI后神经内分泌系统过度激活,循环中AngⅡ、ET1明显升高并导致心脏间质胶原含量的升高。西拉普利通过抑制循环紧素血管紧张素醛固酮系统和内皮素系统,降低AngⅡ和ET1,并通过抑制缓激肽降解,抑制心脏非梗死区间质胶原的过度沉积。阿司匹林对MI后心脏间质胶原的沉积无明显影响。西拉普利与阿司匹林联合应用不影响西拉普利的抑制非梗死区心脏间质胶原过度沉积的作用。
Objective: To observe the effects of cilazapril and aspirin on cardiac interstitial collagen metabolism after experimental myocardial infarction (MI) in rats. Methods: MI model was established by ligation of left anterior descending coronary artery (coronary artery) in rats. The sham group, infarction group, cilazapril group, aspirin group and combination group were established. The level of angiotensin Ⅱ (AngⅡ), 6ketoPGF1α (6ketoPGF1α), endothelin 1 (ET1) and interstitial collagen in the infarcted area, left ventricular non-infarction area and right ventricle were measured 2 weeks after operation. Results: Compared with the sham-operation group, the levels of AngⅡ, ET1 and 6ketoPGF1α were decreased and the contents of collagen in left ventricular non-infarct area and right ventricle were significantly increased. There was no significant difference in the collagen content of infarction area among the experimental groups. Compared with infarction group, blood 6ketoPGF1αin aspirin group was significantly lower than that in non-infarcted area and right ventricle. There was no significant difference in collagen content between aspirin group and right ventricle. In cilazapril group, the levels of AngⅡ, ET1 were significantly decreased, while 6ketoPGF1αlevel Non-infarct area and right ventricular collagen content was significantly reduced. Compared with cilazapril group, 6ketoPGF1α was significantly decreased in the combination group, while there was no significant difference in collagen content in non-infarcted area and right ventricle. Conclusion: The neuroendocrine system is over-activated after MI, and the levels of AngⅡ and ET1 are significantly increased in the circulation and lead to the increase of cardiac interstitial collagen content. Cilazapril reduces angiotensin-aldosterone system and endothelin system by inhibiting the circulating tight-catenin and inhibits angiotensin II and ET1 by inhibiting the degradation of bradykinin, inhibiting the excessive deposition of collagen in non-infarcted area of the heart. Aspirin had no significant effect on the deposition of cardiac interstitial collagen after MI. The combination of cilazapril and aspirin did not affect the effect of cilazapril on inhibiting the excessive deposition of cardiac interstitial collagen in non-infarcted areas.