Kondo M, Yoshikawa T, Takemura S, Yokoe N, Kawai K, Masuda M
Digestion. 1978;17(1):38-45. doi: 10.1159/000198092.
Disseminated intravascular coagulation (DIC), experimentally induced by endotoxin, caused severe hemorrhagic necrosis of the intestinal mucosa in dogs. Microscopic observation showed tortuous thrombus formation in the microcirculation of the villi. Ligation of the pancreatic and bile ducts, or administration of heparin protected the mucosa from hemorrhagic necrosis, while systemic administration of tranexamic acid increased the intestinal mucosal lesion. Local pretreatment of the intestinal mucosa by Trasylol or tranexamic acid reduced the degree of hemorrhagic necrosis. It is concluded that intravascular coagulation in the microcirculation of the intestinal mucosa, as well as pancreatic proteases, play a role in the pathogenesis of hemorrhagic necrosis in the intestine associated with DIC.
内毒素实验性诱导的弥散性血管内凝血（DIC）可导致犬肠道黏膜严重出血性坏死。显微镜观察显示绒毛微循环中形成了迂曲的血栓。结扎胰管和胆管或给予肝素可保护黏膜免受出血性坏死，而全身给予氨甲环酸则会加重肠道黏膜损伤。用抑肽酶或氨甲环酸对肠黏膜进行局部预处理可减轻出血性坏死程度。得出的结论是，肠黏膜微循环中的血管内凝血以及胰腺蛋白酶在与DIC相关的肠道出血性坏死发病机制中起作用。
