Koike Marcia Kiyomi, Frimm Clovis De Carvalho, Cúri Mariana
LIM 51 - Laboratory of Emergency Medicine, University of São Paulo Medical School, São Paulo, SP, Brazil.
Int J Exp Pathol. 2007 Aug;88(4):279-90. doi: 10.1111/j.1365-2613.2007.00540.x.
Subendocardial remodelling of the left ventricular (LV) non-infarcted myocardium has been poorly investigated. Previously, we have demonstrated that low coronary driving pressure (CDP) early postinfarction was associated with the subsequent development of remote subendocardial fibrosis. The present study aimed at examining the role of CDP in LV remodelling and function following infarction. Haemodynamics were performed in Wistar rats immediately after myocardial infarction (MI group) or sham surgery (SH group) and at days 1, 3, 7 and 28. Heart tissue sections were stained with HE, Sirius red and immunostained for alpha-actin. Two distinct LV regions remote to infarction were examined: subendocardium (SE) and interstitium (INT). Myocyte necrosis, leucocyte infiltration, myofibroblasts and collagen volume fraction were determined. Compared with SH, MI showed lower CDP and LV systolic and diastolic dysfunction. Necrosis was evident in SE at day 1. Inflammation and fibroplasia predominated in SE as far as day 7. Fibrosis was restricted to SE from day 3 on. Inflammation occurred in INT at days 1 and 3, but at a lower grade than in SE. CDP correlated inversely with SE necrosis (r = -0.65, P = 0.003, at day 1), inflammation (r = -0.76, P < 0.001, at day 1), fibroplasia (r = -0.47, P = 0.04, at day 7) and fibrosis (r = -0.83, P < 0.001, at day 28). Low CDP produced progressive LV expansion. Necrosis at day 1, inflammation at days 3 and 7, and fibroplasia at day 7 correlated inversely with LV function. CDP is a key factor to SE integrity and affects LV remodelling and function following infarction.
左心室（LV）非梗死心肌的心内膜下重塑研究较少。此前，我们已经证明，心肌梗死后早期的低冠状动脉驱动压力（CDP）与随后远处心内膜下纤维化的发展有关。本研究旨在探讨CDP在心肌梗死后左心室重塑和功能中的作用。在Wistar大鼠心肌梗死（MI组）或假手术（SH组）后立即以及术后第1、3、7和28天进行血流动力学检测。心脏组织切片用苏木精-伊红（HE）染色、天狼星红染色，并进行α-肌动蛋白免疫染色。检查两个远离梗死灶的不同左心室区域：心内膜下（SE）和间质（INT）。测定心肌细胞坏死、白细胞浸润、肌成纤维细胞和胶原体积分数。与SH组相比，MI组的CDP较低，左心室收缩和舒张功能障碍。第1天SE区可见明显坏死。直至第7天，SE区以炎症和纤维增生为主。从第3天开始，纤维化局限于SE区。第1天和第3天INT区出现炎症，但程度低于SE区。CDP与SE坏死（第1天，r = -0.65，P = 0.003）、炎症（第1天，r = -0.76，P < 0.001）、纤维增生（第7天，r = -0.47，P = 0.04）和纤维化（第28天，r = -0.83，P < 0.001）呈负相关。低CDP导致左心室逐渐扩张。第1天的坏死、第3天和第7天的炎症以及第7天的纤维增生与左心室功能呈负相关。CDP是维持SE完整性的关键因素，并影响心肌梗死后左心室的重塑和功能。
