TIMING AND LOCUS OF VASCULAR PROLIFERATION IN ACUTE MYOCARDIAL INFARCTION

尽管越来越多的证据表明冠状动脉侧支可以防止 或限制心肌梗死的大小， 这些侧枝发育。 而正常人、猪和老鼠的心脏 只有少量的冠状动脉到冠状动脉侧支，3到 40微米大小，正常的狗心脏侧枝众多， 大小为100-200微米。 针对渐进性狭窄 冠状动脉血管破裂 犬科动物的血管不仅扩张 但通过细胞分裂的过程在所有3个细胞中生长更大， 血管壁的层。 尚不清楚缺血是否 在胚胎发育中会引发小血管增生 和肿瘤血管生成。 在患有冠状动脉疾病的人中， 有时可见大的动脉间侧支循环， 知道这些是否是由于扩大预先存在的 动脉间的小动脉还是它们代表了 毛细血管增生后的血管重塑过程。 因此，作为研究血管增生性 对缺血无梗死的反应，我们研究了早期 对急性心肌梗死的增殖反应 结扎大鼠冠状动脉。 在非手术和假手术组中， 我们的控制是为了确认非常低的细胞水平， 在正常的心脏中增殖。 然而， 标记开始于梗塞边缘区的48小时， 成纤维细胞和毛细血管和小静脉内皮细胞。 了48 小时，有强烈的标记，延伸到非- 发炎的非缺血性组织，只在 毛细血管和小静脉。 这些数据表明，在 心肌梗死新生血管形成开始非常早， 主要存在于毛细血管和小静脉中，如肿瘤中的情况 血管生成 这表明细胞生理学和 血管生成的生物化学适用于心肌 梗塞 此外，这些生长反应充分发生 迅速地影响诸如梗塞扩展、扩张 或破裂。 目前的研究旨在验证这是否属实 心肌缺血的症状

Despite increasing evidence that coronary collaterals can prevent or limit the size of myocardial infarction it is not known how these collaterals develop. Whereas normal human pig and rat hearts have only a small number of coronary to coronary collaterals, 3 to 40 microns in size, normal dog heart collaterals are numerous and are 100-200 microns in size. In response to progressive narrowing of a coronary vessel over 5 days. canine vessels not only dilate but grow larger by a process involving cell division in all 3, layers of the vessel wall. It is not known whether ischemia triggers small vessel proliferation that is seen in embryogenesis and tumor angiogenesis. In humans with coronary artery disease, large interarterial collaterals are sometimes seen but it is not known whether these are due to expansion of pre-existing interarterial arterioles or whether they represent the final process of vascular remodeling following capillary proliferation. Therefore, as a preliminary step to studying the vasoproliferative response to ischemia without infarction, we studied the early proliferative response to acute myocardial infarction produced by coronary ligation in rats. In the nonoperated and sham operated controls we were are to confirm the very lows level of cell proliferation in the normal heart. However, an increase in labeling began by 48 hours in the border zone of the infarct, in fibroblasts and capillary and venular endothelial cells. By 48 hours there was intense labeling which extended into the non- inflamed nonischemic tissue, where it was seen only in the capillaries and venules. Thus, these data suggest that in myocardial infarction neovascularization begins very early and is found mostly in capillaries and venules as is the case in tumor angiogenesis. This suggests that the cellular physiology and biochemistry of angiogenesis are applicable to myocardial infarction. Furthermore, these growth responses occur sufficiently quickly to influence such events as infarct extension, expansion or rupture. Current studies are designed to see if this is true of myocardial ischemia as well.