The impact of pressure overload on coronary vascular changes following myocardial infarction in rats

被引:6
作者
Chen, Jiqiu [1 ]
Petrov, Artiom [2 ]
Yaniz-Galende, Elisa [1 ]
Liang, Lifan [1 ]
de Haas, Hans J. [2 ]
Narula, Jagat [2 ]
Hajjar, Roger J. [1 ]
机构
[1] Mt Sinai Sch Med, Cardiovasc Res Ctr, New York, NY 10029 USA
[2] Mt Sinai Sch Med, Dept Cardiol, New York, NY 10029 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 2013年 / 304卷 / 05期
关键词
myocardial infarction; congestive heart failure; left coronary artery; fibrosis; hypertension; HEART-FAILURE; ISCHEMIA; REPERFUSION; PATHOPHYSIOLOGY; CELLS; HYPERTENSION; INJURY; SIZE;
D O I
10.1152/ajpheart.00793.2012
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Chen J, Petrov A, Yaniz-Galende E, Liang L, de Haas HJ, Narula J, Hajjar RJ. The impact of pressure overload on coronary vascular changes following myocardial infarction in rats. Am J Physiol Heart Circ Physiol 304: H719-H728, 2013. First published December 28, 2012; doi:10.1152/ajpheart.00793.2012.-This study investigates the impact of pressure overload on vascular changes after myocardial infarction (MI) in rats. To evaluate the effect of pressure overload, MI was induced in three groups: 1) left coronary artery ligation for 1 mo (MI-1m), 2) ischemia 30 min/reperfusion for 1 mo (I/R-1m), and 3) ischemia-reperfusion (I/R) was performed after pressure overload induced by aortic banding for 2 mo; 1 mo post-I/R, aortic constriction was released (Ab+I/R+DeAb). Heart function was assessed by echocardiography and in vivo hemodynamics. Resin casting and three-dimensional imaging with microcomputed tomography were used to characterize changes in coronary vasculature. TTC (triphenyltetrazohum chloride) staining and Masson's Trichrome were conducted in parallel experiments. In normal rats, MI induced by I/R and permanent occlusion was transmural or subendocardial. Occluded arterial branches vanished in MI-1m rats. A short residual tail was retained, distal to the occluded site in the ischemic area in I/R-1m hearts. Vascular pathological changes in transmural MI mostly occurred in ischemic areas and remote vasculature remained normal. In pressure overloaded rats, I/R injury induced a sub-MI in which ischemia was transmural, but myocardium in the involved area had survived. The ischemic arterial branches were preserved even though the capillaries were significantly diminished and the pathological changes were extended to remote areas, characterized by fibrosis, atrial thrombus, and pulmonary edema in the Ab+I/R+DeAb group. Pressure overload could increase vascular tolerance to I/R injury, but also trigger severe global ventricular fibrosis and results in atrial thrombus and pulmonary edema.
引用
收藏
页码:H719 / H728
页数:10
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