大鼠胆源性脓毒症时的肝脏糖异生功能及相关激素环境的改变

急性胆源性肝损害所致多系统器官功能不全的机理尚不完全清楚。作者采用肝脏原位灌注法测定了大鼠急性胆道感染（AOC）所致脓毒症时肝脏糖异生功能的改变，并对AOC后机体重要理糖激素环境的变化及其对精异生功能的影响进行了探讨。结果表明：AOC后24小时大鼠肝脏糖异生功能明显降低，血乳酸和促糖激素水平明显升高，胰岛素显著降低，血糖约维持在正常水平的2．5倍。AOC48小时，大鼠肝脏糖异生功能进一步降低，血乳酸浓度继续增加，但促糖激素无继续升高或明显下降，胰岛素显著上升，血糖水平较AOC24小时明显下降。提示AOC早期大鼠肝脏糖异生功能即有明显降低，此时机体可通过增加糖异生基质和改变理糖激素环境维持应激所需要的高血糖水平；后期肝脏糖异生功能进一步受损，机体代偿功能明显紊乱，血糖浓度明显降低，这可能是胆源性多系统辞官功能不全发生发展的病理生理机理之一。

DECREASED GLUCONEOGENESIS OF THE LIVER IN BILIARY SEPSIS AND ITS EFFECT ON SOME RELATED HORMONES

By perfusing livers from Wistar rats rendered sepsis with acute obstructive cholangitis(AOC)in vitro in a nonrecirculating mode, we measured the rates of gluconeogenesis from saturating concentation of lactate (5 mmol/L) plus pyruvate (0.5 mmol/L) and the response of gluconeogenesis to glucagon and epinephrine. We also studied the AOC induced alterations in the milieu of gluconeogenic (glucagon, epinephrine and cortisol) and conterregulatory (insulin) hormones. The results showed the rate of gluconeogenesis of AOC 24 h. proup was significantly reduced and this reduction could be compensated by increases of glucose precursors, especially lactate and of gluconeogenic hormones to a serum glucose level as much as 2.5 times the normal which is needed in stress reaction. The rate of gluconeogenesis of AOC 48 h. was further decreased and this decrease could not be compensated probadly as a result of severe damage to hepatocytes. The results indicate that the reduced glucose metabolic response to AOC may Play an important role in the development of cholangitis-induced dysfunction of multiPle organs.