Peyton M D, Hinshaw L B, Greenfield L J, Elkins R C
Surg Gynecol Obstet. 1975 Nov;141(5):727-30.
Terminal stage, endotoxin shock in the dog is associated with profound hypoglycemia. The response of eviscerated dogs with absent pancreatic and hepatic function is compatible with insulin independent peripheral tissue catabolism of glucose, and an increased lactate-pyruvate ratio suggests anaerobic metabolism. Increased survival in dogs administered exogenous glucose indicates reversible, fuel dependent changes of peripheral tissue metabolism. Since hyperglycemia has been a predominant finding in clinical endotoxin shock, species differences are emphasized, but perhaps closer scrutiny of the terminal stages of clinical endotoxin shock would be more compatible with this experimental model. In any event, an explanation of the metabolic changes in this model may prove valuable in understanding the physiopathology of endotoxin shock.
在犬类中，终末期内毒素休克与严重低血糖相关。对于胰腺和肝功能缺失的去内脏犬，其反应符合葡萄糖的胰岛素非依赖性外周组织分解代谢，而乳酸-丙酮酸比值升高提示无氧代谢。给予外源性葡萄糖的犬存活率增加，表明外周组织代谢存在可逆的、依赖燃料的变化。由于高血糖一直是临床内毒素休克的主要表现，因此强调了物种差异，但也许对临床内毒素休克终末期进行更仔细的研究将与该实验模型更相符。无论如何，对该模型中代谢变化的解释可能对理解内毒素休克的生理病理学有价值。
