PENNER A, KLEIN S H
J Exp Med. 1952 Jul;96(1):59-69. doi: 10.1084/jem.96.1.59.
All analysis of the mechanisms involved in the pathogenesis of the visceral lesions produced by Shiga toxin in the dog has indicated that the structural changes are produced by a vascular mechanism which is under control of the sympathetic nervous system. Paralysis of the latter at the myoneural junction or in the ganglia by means of drugs served to prevent the tissue changes as well as the hyperglycemia and hemoconcentration characteristic of the sympathomimetic response. The observations indicated that the toxin acted via a mechanism located in the central nervous system. Further studies of the action of Shiga toxin by means of cerebral cross-circulation are reported here. In these the cerebral blood flow of one dog derived from the circulation of the trunk and limbs of another. Injection of the toxin into the femoral vein of this latter dog resulted in the appearance of visceral lesions, hemoconcentration, and hyperglycemia in the former whose brain only received blood containing the toxin. The resulting visceral changes were identical with those observed in the intact unanesthetized dog which had received the toxin directly. The observations indicate that, in dogs, Shiga toxin produces its characteristic visceral lesions via the central nervous system. Possible mechanisms are discussed.
所有关于志贺毒素在犬体内引起内脏病变的发病机制分析均表明，结构变化是由一种受交感神经系统控制的血管机制产生的。通过药物使交感神经系统在肌神经接头处或神经节发生麻痹，可预防组织变化以及拟交感反应特有的高血糖和血液浓缩。这些观察结果表明，毒素是通过位于中枢神经系统的一种机制起作用的。本文报道了通过脑交叉循环对志贺毒素作用的进一步研究。在这些研究中，一只犬的脑血流来自另一只犬的躯干和四肢的循环。将毒素注入后一只犬的股静脉，导致前一只犬出现内脏病变、血液浓缩和高血糖，而前一只犬的脑仅接受含有毒素的血液。所产生的内脏变化与直接接受毒素的完整未麻醉犬所观察到的变化相同。这些观察结果表明，在犬体内，志贺毒素通过中枢神经系统产生其特征性的内脏病变。文中讨论了可能的机制。
