Kobori K, Suzuki K, Yoshida Y, Ooneda G
Virchows Arch A Pathol Anat Histol. 1979 Dec;385(1):29-39. doi: 10.1007/BF00433538.
Experimental contraction was produced in the rat mesenteric arteries and the arterial segments were studied morphologically. When the rat mesenteric artery was exposed in physiological saline solution at 37 degrees C and 2-3 mg of methoxamine hydrochloride (10 mg/ml) was dripped onto it, intense contraction was observed for about 30 min but elevation in blood pressure was slight. During the contraction, numerous vacuoles were seen in the medial smooth muscle cells of the arterial segments, and these vacuoles were shown electron microscopically to have double unit membranes, indicating that they were formed by herniation of a part of the adjacent smooth muscle cell body. In the arteries 1-6 h after the end of the contraction, cellular, nuclear and vacuolar membranes and myofilaments of the medial muscle cells were partially lost. 12-24 h after the contraction the arteries exhibited necrosis and desquamation of endothelial cells and platelet adhesion. In the media, smooth muscle cells were completely deprived of cell membranes, myofilaments, nuclei, intracytoplasmic organelles other than mitochondria, and vacuolar membranes. The cytoplasm was filled with fine granular and granulo-vesicular material, and fibrin insudation was observed in these severely damaged cells. Arterial contraction may be an important factor in the induction of arterial lesions.
在大鼠肠系膜动脉中引发实验性收缩，并对动脉节段进行形态学研究。当大鼠肠系膜动脉在37℃的生理盐溶液中暴露，且向其上滴加2 - 3毫克盐酸美索明（10毫克/毫升）时，观察到强烈收缩约30分钟，但血压升高轻微。在收缩过程中，动脉节段的中膜平滑肌细胞内可见大量空泡，电子显微镜显示这些空泡具有双层单位膜，表明它们是由相邻平滑肌细胞体的一部分疝出形成的。在收缩结束后1 - 6小时的动脉中，中膜平滑肌细胞的细胞膜、细胞核、空泡膜和肌丝部分丧失。收缩后12 - 24小时，动脉出现内皮细胞坏死和脱落以及血小板黏附。在中膜，平滑肌细胞完全失去细胞膜、肌丝、细胞核、除线粒体之外的胞质细胞器以及空泡膜。细胞质充满细颗粒和颗粒 - 小泡物质，在这些严重受损的细胞中观察到纤维蛋白渗出。动脉收缩可能是诱导动脉病变的一个重要因素。
