Effects of captopril on contractility after myocardial infarction: experimental observations.
Effects of captopril on contractility after myocardial infarction: experimental observations.
复制标题
卡托普利对心肌梗塞后收缩力的影响：实验观察。
DOI：
10.1016/0002-9149(91)90258-m
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Goldman,S
中科院分区：
文献类型：
--
作者：
Litwin,SE;Raya,TE;Warner,A;Litwin,CM;Goldman,S
大面积心肌梗死后，左心室（LV）功能受损和外周循环改变导致慢性充血性心力衰竭综合征。虽然血管紧张素转换酶抑制剂治疗可改善心血管功能，但很难确定这种益处是否是由于器官与肌肉功能的变化。通过结扎左冠状动脉建立的心力衰竭大鼠模型导致的病理生理学与患者中观察到的相似，即LV舒张末期压和容积增加、非梗死心肌肥大、LV舒张时间常数延长、静脉顺应性降低和总血容量增加。在非梗死性乳头肌，从心力衰竭大鼠分离，最大发达国家的紧张和紧张上升的峰值速率（+ DT DT）下降，时间峰值紧张延长，心肌硬度增加。形态学变化包括乳头肌肌细胞横截面积增加和心肌羟脯氨酸含量增加。Captopril（2 g/L饮用水）通过降低动脉压、增加静脉顺应性和减少血容量来改变LV负荷。这导致LV舒张末期压和容量降低。在非梗死心肌中，达到峰值张力的时间缩短，而发达的张力，+ dT dt和肌肉僵硬度仍然异常。开搏通降低肌细胞横截面积，但胶原蛋白含量仍然升高。因此，在心力衰竭的大鼠梗死模型中，用卡托普利治疗改变了LV重构和肥大，但仅产生肌肉功能的适度改善。在该模型中，治疗3周后，似乎血管紧张素转换酶抑制的主要益处是由于负荷条件变化导致的器官功能改善，而肌肉功能仍然受损。
After large myocardial infarction, compromised left ventricular (LV) function and changes in the peripheral circulation result in the syndrome of chronic congestive heart failure. Although treatment with angiotensin-converting enzyme inhibitors improve cardiovascular function, it is difficult to determine whether this benefit is due to changes in organ versus muscle function. The rat model of heart failure, created by ligating the left coronary artery, results in pathophysiology that is similar to that seen in patients, ie, increased LV end-diastolic pressure and volume, hypertrophy of the noninfarcted myocardium, prolongation of the time constant of LV relaxation, decreased venous compliance, and increased total blood volume. In noninfarcted papillary muscles, isolated from rats with heart failure, maximal developed tension and peak rate of tension rise (+ dT dt) are decreased, time to peak tension is prolonged, and myocardial stiffness is increased. Morphologic changes include an increase in papillary muscle myocyte cross-sectional area and an increase in myocardial hydroxyproline content. Captopril (2 g/liter drinking water) alters LV loading by decreasing arterial pressure, increasing venous compliance, and decreasing blood volume. This results in a decrease in LV end-diastolic pressure and volume. In the noninfarcted myocardium, time to peak tension is shortened, whereas developed tension,+ dT dt, and muscle stiffness remain abnormal. Captopril decreases myocyte cross-sectional area, but collagen content remains elevated. Thus, in the rat infarct model of heart failure, treatment with captopril alters LV remodeling and hypertrophy but produces only modest improvement in muscle function. In this model, after treatment for 3 weeks, it appears that the major benefit from angiotensin-converting enzyme inhibition is due to improvements in organ function resulting from changes in loading conditions, whereas muscle function remains compromised.