Johnson R C, Crissman R S, DiDio L J
Lab Invest. 1979 Feb;40(2):183-93.
Transmural infarcts of the ventrolateral wall of canine left ventricle were produced by ligation of the ventral interventricular (anterior descending) branch of the left coronary artery. Endocardium from these infarcted hearts was sampled at sites corresponding to the infarct center and periphery, and to uninfarcted (normal) area at 24 and 48 hours after ligation, and examined by correlative scanning and transmission electron microscopy and by light microscopy. Endocardial samples from sham-ligated hearts were included as a further control. Striking alterations were observed in the endocardium that lined infarcted myocardium. There was endothelial desquamation coextensive with leukocytic invasion. Leukocytes appeared to initiate sloughing by separating the endothelial cells from their basal lamina and partially from one another. The latter cells desquamated in sheets, leaving behind a denuded basal lamina. Although altered in form, the individual endothelial cells seemed to remain largely intact. Denuded subendothelial surfaces only rarely contained thrombi. In areas where the cardiac endothelium was altered, the subjacent subendocardium, myocardium, and usually the remainder of the endocardium also showed leukocytic exudate. Samples from uninfarcted regions showed an intact, leukocyte-free endocardium, as did the sham-ligated controls. The appearance of abnormal endocardium was qualitatively similar wherever found, whether in different areas of the same heart or from one heart to another, and regardless of age of infarct. In 48-hour infarcts, almost all of the central and most of the peripheral samples exhibited the changes described. The data suggested a similar pattern for hearts with 24-hour infarcts. By locating biopsy sites in frozen cardiac sections processed for histologic staining and 201-thallium autoradiography, the electron microscopy results were shown to correlate with the intramural histopathologic topography of the infarcts. The alterations described here represent the endocardial manifestation of the inflammatory stage of transmural infarcts, known to be well developed in 1- and 2-day-old lesions.
通过结扎左冠状动脉的室间前降支，制造犬左心室前外侧壁透壁性梗死。在结扎后24小时和48小时，从这些梗死心脏的心内膜对应梗死中心、周边以及未梗死（正常）区域取样，并通过相关的扫描电子显微镜、透射电子显微镜及光学显微镜进行检查。将假结扎心脏的心内膜样本作为进一步对照。在梗死心肌表面的心内膜观察到显著改变。内皮细胞脱落与白细胞浸润范围一致。白细胞似乎通过将内皮细胞与其基膜分离并部分相互分离来引发脱落。后者成片脱落，留下裸露的基膜。尽管形态改变，但单个内皮细胞似乎基本保持完整。裸露的内皮下表面很少有血栓。在心脏内皮细胞发生改变的区域，其下方的心内膜下层、心肌以及通常心内膜的其余部分也有白细胞渗出。未梗死区域的样本以及假结扎对照的心内膜均完整且无白细胞。无论在同一心脏的不同区域、不同心脏，还是梗死的不同时间，异常心内膜的表现本质上相似。在48小时梗死的样本中，几乎所有中央和大部分周边样本都呈现出上述变化。数据表明24小时梗死的心脏也有类似模式。通过在经组织学染色和铊 - 201放射自显影处理的冷冻心脏切片中定位活检部位，电子显微镜结果显示与梗死灶壁内组织病理学特征相关。这里描述的改变代表了透壁性梗死炎症阶段的心内膜表现，已知在1天和2天的病变中充分发展。
