Thai H M, Van H T, Gaballa M A, Goldman S, Raya T E
Department of Internal Medicine, Veterans Affairs Medical Center and Sarver Heart Center, University of Arizona, Tucson, Arizona 85723, USA.
Am J Physiol. 1999 Mar;276(3):H873-80. doi: 10.1152/ajpheart.1999.276.3.H873.
Angiotensin II type 1 (AT1) receptor blockade attenuates myocardial fibrosis after myocardial infarction (MI). However, whether inhibition of fibrosis by AT1 receptor blockade influences myocardial stiffness and contractility is unknown. We measured left ventricular (LV) hemodynamics, papillary muscle function, and myocardial stiffness and fibrosis in rats randomized to losartan or placebo 1 day after MI and treated subsequently for 8 wk. Losartan decreased LV and right ventricular weights as well as mean aortic and LV systolic pressures in sham and MI rats. LV end-diastolic pressure increased after MI and was decreased with losartan. Maximal developed tension and peak rate of tension rise and decline were decreased in MI vs. sham rats. Interstitial fibrosis developed after MI and was prevented in losartan-treated MI rats. The development of abnormal myocardial stiffness after MI was prevented by losartan. After MI, AT1 receptor blockade prevents an abnormal increase in myocardial collagen content. This effect was associated with a normalization of passive myocardial stiffness.
血管紧张素II 1型（AT1）受体阻断可减轻心肌梗死后的心肌纤维化。然而，AT1受体阻断对纤维化的抑制是否会影响心肌僵硬度和收缩性尚不清楚。我们对心肌梗死后1天随机给予氯沙坦或安慰剂并随后治疗8周的大鼠进行了左心室（LV）血流动力学、乳头肌功能以及心肌僵硬度和纤维化的测量。氯沙坦降低了假手术组和心肌梗死组大鼠的左心室和右心室重量以及平均主动脉压和左心室收缩压。心肌梗死后左心室舒张末期压力升高，而氯沙坦可使其降低。与假手术组大鼠相比，心肌梗死组大鼠的最大张力发展、张力上升和下降的峰值速率降低。心肌梗死后出现间质纤维化，而氯沙坦治疗的心肌梗死组大鼠可预防此现象。氯沙坦可预防心肌梗死后异常心肌僵硬度的发展。心肌梗死后，AT1受体阻断可防止心肌胶原含量异常增加。这种作用与被动心肌僵硬度的正常化有关。
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