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本文采用大鼠心肌梗塞（ＭＩ）模型观察开搏通干预对心肌细胞肥大、心室各部位胶原含量、总量、Ｉ、Ⅲ型胶原蛋白比值（Ｉ／Ⅲ（Ｐ）及Ｉ、Ⅲ型胶原ｍＲＮＡ比值（Ｉ／Ⅲ（Ｒ））的影响。结果表明：（１）开搏通在阻抑ＭＩ大鼠左室非梗塞区（ＮＩＡ）及右室（ＲＶ）心肌细胞肥大的同时对心室各部位胶原基质改建的影响不同。开搏通不仅能够完全阻抑ＮＩＡ胶原基质的增生，且能使Ｉ／Ⅲ（Ｐ）降至对照水平；对ＲＶ仅使胶原总量相应减少，而对Ｉ／Ⅲ（Ｐ）无明显影响；对梗塞区（ＩＡ）胶原基质的改建则无明显影响。（２）Ｉ／Ⅲ（Ｒ）的变化规律与Ｉ／Ⅲ（Ｐ）变化一致。结果揭示：（１）不同类型的心肌肥大中，胶原改建的调控机制可能不同。心肌细胞肥大的抑制并不一定伴有同步的胶原基质改变；（２）开搏通对胶原基质改建的作用可能与其降低ＡｎｇⅡ水平，从而在基因表达水平影响了ＦＢＣ的胶原合成有关。
In this paper, the myocardial infarction (MI) model was used to observe the effects of Caifei on cardiomyocytes hypertrophy, ventricular collagen content, total, type I and type III collagen ratio (I / III (P) Ratio (I / III (R)) .Results showed that: (1) Captopril could inhibit the myocardial hypertrophy in left ventricular non-infarct zone (NIA) and right ventricle (RV) The effect of collagen matrix remodeling was different. Camptothecine not only completely inhibited the proliferation of NIA collagen matrix, but also reduced I / III (P) to the control level; RV only reduced the total amount of collagen, (P) had no significant effect on the remodeling of collagen matrix in infarcted area (IA). (2) The change of I / III (R) was consistent with that of I / Different types of myocardial hypertrophy, the regulation of collagen remodeling may be different mechanisms of inhibition of myocardial cell hypertrophy is not necessarily accompanied by synchronous collagen matrix changes; (2) Caifei on collagen matrix changes Damage associated with decreased levels AngⅡ, thus affecting the collagen synthesis in FBC relevant level of gene expression.