Ownby C L, Kainer R A, Tu A T
Am J Pathol. 1974 Aug;76(2):401-14.
The pathogenesis of hemorrhage induced by rattlesnake (Crotalus atrox) venom was investigated at the electron microscopic level. Swiss-Webster white mice were injected intramuscularly with one-fifth the LD(50) dose of whole venom. Muscle samples were obtained by biopsy 2 minutes, 30 minutes and 3 hours after venom injection. Capillaries in the endomysium were in various stages of degeneration. Endothelial cells of damaged capillaries contained dilatated endoplasmic reticulum and perinuclear space, and, in many cases, swollen cytoplasm. Blebbing of endothelial cytoplasm of swollen and nonswollen cells was observed. These changes were followed by rupture of the plasma membrane which resulted in the subsequent extravasation of blood. Platelet aggregations plugged gaps in vessel walls and often completely occluded the lumina of capillaries. The experimental injection of rattlesnake venom induced hemorrhage by rhexis. The same or a similar pathogenesis is probably responsible for hemorrhage which occurs in actual snakebite cases.
在电子显微镜水平上研究了响尾蛇(变色蛇)毒液诱导出血的发病机制。将瑞士韦伯斯特小白鼠肌肉注射五分之一半数致死量(LD50)的全毒液。在毒液注射后2分钟、30分钟和3小时通过活检获取肌肉样本。肌内膜中的毛细血管处于不同程度的退化阶段。受损毛细血管的内皮细胞含有扩张的内质网和核周间隙,并且在许多情况下,细胞质肿胀。观察到肿胀和未肿胀细胞的内皮细胞质有泡状突起。这些变化随后导致质膜破裂,进而导致血液外渗。血小板聚集堵塞血管壁的间隙,常常完全阻塞毛细血管腔。响尾蛇毒液的实验性注射通过破裂诱导出血。实际蛇咬伤病例中发生的出血可能是由相同或相似的发病机制引起的。