Department of Biomedical Sciences, New York Institute of Technology College of Osteopathic Medicine, Rockefeller Building, Room 215E, Northern Boulevard, Old Westbury, NY 11568-8000, USA.
Biol Sex Differ. 2014 Jan 3;5(1):1. doi: 10.1186/2042-6410-5-1.
An increasing body of evidence indicates that left ventricular (LV) remodeling, especially the degree of reactive myocardial hypertrophy after myocardial infarction (MI), differs in males and females. Surprisingly, to date, the sex-specific post-MI alterations of the coronary vasculature remain undetermined. Therefore, we tested the hypothesis that adaptive coronary arteriolar and capillary modifications occurring in response to reactive myocyte hypertrophy differ between middle-aged male and female post-MI rats.
A large MI was induced in 12-month-old male (M-MI) and female (F-MI) Sprague-Dawley rats by ligation of the left coronary artery. Four weeks after surgery, rats with transmural infarctions, greater than 50% of the LV free wall (FW), were evaluated. Sham-operated male (M-Sham) and female (F-Sham) rats served as an age-matched controls.
F-MI and M-MI rats had similar sized infarcts (61.3% ± 3.9% vs. 61.5% ± 1.2%) and scale of LV remodeling, as indicated analogous remodeling indices (1.41 ± 0.11 vs. 1.39 ± 0.09). The degree of reactive post-MI myocardial hypertrophy was adequate to normalize LV weight-to-body weight ratio in both sexes; however, the F-MI rats, in contrast to males, showed no myocyte enlargement in the LVFW epimyocardium. At the same time, a greater than 50% expansion of myocyte area in the male epimyocardium and in the female endomyocardium was accompanied by a 23% (P < 0.05) increase in capillary-to-myocyte ratio, indicative of adaptive angiogenesis. Based on arteriolar length density in post-MI hearts, the resistance vessels grew in the male LVFW as well as the septum by 24% and 29%, respectively. In contrast, in females, a significant (30%) expansion of arteriolar bed was limited only to the LVFW. Moreover, in F-MI rats, the enlargement of the arteriolar bed occurred predominantly in the vessels with diameters <30 μm, whereas in M-MI rats, a substantial (two- to threefold) increase in the density of larger arterioles (30 to 50 μm in diameter) was also documented.
Our data reveal that while both sexes have a relatively similar pattern of global LV remodeling and adaptive angiogenesis in response to a large MI, male and female middle-aged rats differ markedly in the regional scale of reactive cardiac myocyte hypertrophy and adaptive arteriogenesis.
越来越多的证据表明，左心室（LV）重构，尤其是心肌梗死后的反应性心肌肥厚程度，在男性和女性中存在差异。令人惊讶的是，迄今为止，心肌梗死后冠状动脉血管的性别特异性改变仍未确定。因此，我们检验了这样一个假设，即在反应性心肌细胞肥大的情况下，发生的适应性冠脉小动脉和毛细血管改变在中年雄性和雌性心肌梗死后大鼠中存在差异。
通过结扎左冠状动脉，在 12 个月大的雄性（M-MI）和雌性（F-MI）Sprague-Dawley 大鼠中诱导大面积心肌梗死。手术后 4 周，评估具有穿透性梗死、LV 游离壁（FW）大于 50%的大鼠。假手术雄性（M-Sham）和雌性（F-Sham）大鼠作为年龄匹配的对照组。
F-MI 和 M-MI 大鼠的梗死大小相似（分别为 61.3%±3.9%和 61.5%±1.2%），LV 重构的程度也相似，表明类似的重构指数（分别为 1.41±0.11 和 1.39±0.09）。反应性心肌梗死后心肌肥厚的程度足以使两性的 LV 重量与体重比正常化；然而，与雄性相比，F-MI 大鼠的 LVFW 心外膜心肌细胞没有增大。与此同时，雄性心外膜和雌性心内膜的心肌细胞面积增加超过 50%，同时毛细血管与心肌细胞的比例增加了 23%（P<0.05），提示适应性血管生成。基于心肌梗死后心脏中小动脉长度密度，雄性 LVFW 和室间隔的阻力血管分别增加了 24%和 29%。相比之下，在雌性中，小动脉床的显著（30%）扩张仅限于 LVFW。此外，在 F-MI 大鼠中，小动脉床的扩大主要发生在直径<30μm的血管中，而在 M-MI 大鼠中，直径为 30 至 50μm的较大小动脉的密度也显著增加（增加了两到三倍）。
我们的数据表明，尽管两性在大面积心肌梗死后都有相对相似的整体 LV 重构和适应性血管生成模式，但中年雄性和雌性大鼠在反应性心肌肥厚和适应性动脉生成的区域性程度上存在显著差异。
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