Bardakhch'ian E A, Lomov Iu M, Gusatinskiĭ I A
Arkh Patol. 1993 Jan-Feb;55(1):29-34.
The 10-12-day suckling rabbits received culture of V. el tor into the stomach, and the ultrastructural changes of intraganglionic capillaries and nervous elements of small intestine were studied in the course of experimental cholera. It was established that the initial changes 1.5 hrs after the beginning of the experiment were characterized by permeability increase, thrombohemorrhagic syndrome development, oedema of endotheliocytes and perivascular space, fibrin precipitation. There were reactive changes in neurons, but alterations in synapses were absent. In the period of cholera vibrio adhesion (4 hrs) the new signs of endothelial cells desquamation developed. At the same time haemorrhages became more distinct and cells of extravasates more diverse. The development of experimental cholera (1-2 days) was accompanied by appearance of large numbers of coated vesicles in endothelium, tight junctions damage and endothelial cells destruction, extensive dysendothelization which promoted blood cells contact with collagen. In this period dystrophic changes progressed in neurons and activation of cholinergic synapses took place. Enhancement of transepithelial transport of liquid, induced by cholera toxin, is partly connected with activation of cholinergic mechanisms in autonomic ganglia of the small intestine.
将10 - 12日龄的哺乳兔经胃接种埃尔托弧菌，在实验性霍乱病程中研究小肠神经节内毛细血管和神经成分的超微结构变化。结果表明，实验开始后1.5小时的初始变化表现为通透性增加、血栓出血综合征形成、内皮细胞和血管周围间隙水肿、纤维蛋白沉淀。神经元有反应性变化，但突触无改变。在霍乱弧菌黏附期（4小时），出现了内皮细胞脱落的新迹象。与此同时，出血更加明显，渗出物细胞更加多样。实验性霍乱的发展（1 - 2天）伴随着内皮细胞中大量被膜小泡的出现、紧密连接损伤和内皮细胞破坏、广泛的内皮脱失，这促进了血细胞与胶原接触。在此期间，神经元发生营养不良性变化，胆碱能突触激活。霍乱毒素诱导的液体跨上皮转运增强，部分与小肠自主神经节中胆碱能机制的激活有关。
