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用失血再灌流加内毒素造成多器官衰竭（ＭＯＦ）的方法，在３００～１５００倍显微镜下观察血小板粘附和内皮损伤的改变，探讨血小板粘附和血管内皮损伤对微循环的影响。结果表明ＭＯＦ早期细静脉内皮上除有较多血小板贴壁或粘附在变形性差的白细胞上，细动脉内皮增厚，内皮表面出现较多血小板粘附，管腔内壁粗糙，可见到血流中的血小板迅速地粘附在损伤的内皮上，堆积、溶合形成壁栓。管腔内还有纤维蛋白形成丝网状粘附在血管腔的中间。血小板和纤维蛋白缠络在一起，形成棉絮状的团块在血管内流动。ＭＯＦ的早期细静脉内皮水肿、管壁增厚并有空泡形成，大的空泡占满整个管腔，造成血流受阻。这些改变都是造成ＭＯＦ发生的重要原因。
The effects of platelet adhesion and endothelial injury on the microcirculation were observed with a microscope at 300 ~ 1500 times microscope. The changes of platelet adhesion and endothelial injury were observed by means of hemorrhage-reperfusion and endotoxin-induced multiple organ failure (MOF). The results showed that in addition to more platelet adherent or adherent to the poorly deformable leukocytes on the arteriole in the early stage of MOF, the thickening of the arterioles’ endothelium and the presence of more platelet adhesion on the endothelium resulted in rough lumen wall and visible blood flow The platelets rapidly adhere to the damaged endothelium, accumulate and dissolve to form wall plugs. Fibrin within the lumen also formed a mesh-like adhesion in the middle of the vascular lumen. Platelets and fibrin tangle together to form a cotton-like mass in the blood vessels. In the early stages of MOF, the endothelial cells were edematous, with thickened walls and vacuoles. Large vacuoles filled the entire lumen and blocked blood flow. These changes are all important factors that cause MOF.