GREISMAN S E
J Exp Med. 1960 Aug 1;112(2):257-78. doi: 10.1084/jem.112.2.257.
Unanesthetized immature albino rabbits exposed to 2 hours of severe but reversible hemorrhagic shock induced with aseptic precautions by multiple cardiac bleedings exhibited no increase in susceptibility to single intravenous injections of 200 microg./kg. E. coli endotoxin administered 4 hours post retransfusion, a quantity of endotoxin that was found to be the largest dose uniformly non-lethal to normal rabbits. Paired and randomly selected rabbits treated identically except for the additional procedure of a femoral arterial cutdown and ligation (without aseptic precautions) exhibited increases in susceptibility to the same endotoxin of several hundredfold. This effect could not be attributed to the femoral cutdown and arterial ligation alone since such trauma when coupled with sham cardiac bleedings failed to increase susceptibility to 200 microg./kg. of endotoxin. These data appear valid since sham cardiac bleedings produced no detectable impairment of myocardial contractility, while 2 hours of hemorrhagic shock at 50 mm. Hg with the Lamson reservoir technique caused an increase in endotoxin susceptibility comparable to that seen when cardiac bleedings were combined with a non-sterile femoral arterial cutdown and ligation. The mechanisms increasing the susceptibility to E. coli endotoxin were investigated. It was found that (a) rabbit femoral skeletal muscle is normally contaminated with clostridia, (b) the use of aseptic femoral wounding precautions exerted some suggestive protective influence, (c) the use of aseptic wounding precautions combined with immediate topical sulfanilamide and wound closure exerted a significant protective influence, and (d) prophylactic polyvalent gas gangrene antitoxin protected in a manner not demonstrable when diphtheria antitoxin was employed as a control. These observations suggest that clostridial wound infection is one mechanism whereby a femoral arterial cutdown lowers endotoxin resistance of the rabbit following hemorrhagic shock. It is, however, not the only mechanism since the ligation of a femoral artery during hemorrhagic shock led to edema following retransfusion equivalent to a mean of approximately 30 per cent of the original circulating plasma volume. The intensification of shock caused by this transudation presumably intensified reticulo-endothelial injury, and thus further lowered the resistance of the rabbit to an intravenous injection of endotoxin 4 hours following retransfusion.
未麻醉的幼龄白化兔，通过多次心脏放血在无菌条件下诱导出严重但可逆的失血性休克2小时，在输血后4小时单次静脉注射200微克/千克大肠杆菌内毒素，其易感性并未增加，该内毒素剂量被发现是对正常兔均一非致死的最大剂量。除了增加股动脉切开和结扎这一额外操作（无无菌预防措施）外，配对并随机选择的兔接受相同处理，结果显示其对相同内毒素的易感性增加了数百倍。这种效应不能仅归因于股动脉切开和结扎，因为当这种创伤与假心脏放血相结合时，未能增加对200微克/千克内毒素的易感性。这些数据似乎是有效的，因为假心脏放血未产生可检测到的心肌收缩力损害，而使用拉姆森储液器技术在50毫米汞柱下进行2小时失血性休克导致内毒素易感性增加，与心脏放血结合非无菌股动脉切开和结扎时所见相当。对增加大肠杆菌内毒素易感性的机制进行了研究。结果发现：（a）兔股部骨骼肌通常被梭菌污染；（b）采取无菌股部创伤预防措施有一定的提示性保护作用；（c）采取无菌创伤预防措施并立即局部应用磺胺类药物和伤口闭合有显著的保护作用；（d）预防性多价气性坏疽抗毒素有保护作用，而以白喉抗毒素作为对照时则未显示出这种作用。这些观察结果表明，梭菌伤口感染是股动脉切开降低失血性休克后兔对内毒素抵抗力的一种机制。然而，这不是唯一的机制，因为失血性休克期间股动脉结扎导致输血后水肿，相当于平均约为原始循环血浆量的30%。这种渗出引起的休克加重可能加剧了网状内皮损伤，从而进一步降低了兔在输血后4小时对静脉注射内毒素的抵抗力。
