地塞米松改变胆源性脓毒症时宿主糖代谢反应

将４０只日本大耳白兔随机分为胆源性脓毒症组（ｎ＝１５，以下简称非治疗组）、地塞米松治疗组（ｎ＝１５）和正常对照组（ｎ＝１０），并将前两组复制成胆源性脓毒症模型。治疗组于伤后３和２４小时按１０ｍｇ／ｋｇ剂量分两次腹腔注射地塞米松，动态检测和比较三组动物血糖水平的变化，用原代肝细胞培养法分析伤后４８小时感染肝叶和非感染肝叶肝细胞糖异生功能。结果显示；伤后２４小时起，非治疗组血糖水平持续显著降低，而治疗组至伤后４８小时才出现血糖降低；伤后４８小时，治疗组感染肝叶肝细胞糖异生的基础速率及激素刺激速率与非治疗组无显著性差异，但非感染肝叶肾上腺素和胰高糖素刺激的肝细胞糖异生速率分别较非治疗组提高了２５．０％和４６．０％，然而两者仍低于正常对照组水平。本实验结果表明，地塞米松对胆源性脓毒症时宿主糖代谢的稳态具有保护效应。

ALTERATION OF GLUCOSE DYSHOMEOSTASIS BY DEXAMETHASONE DURING BILIARY SEPSIS IN THE RABBIT

This study examined the effects of dexamethasone on binary sepsis-induced hypoglycemia and hepatic gluconeogenesis depression in fasting rabbits. Dexamethasone was administered intraveneously with a dose of 10mg/kg body weight at 3h and 24h following septic challenge. Binary sepsis caused severe hypoglycemia in the rat since 24h after septic challenge. Dexamethasone delayed the development of hypoglycemia in the rabbit till 48h after septic challenge. Hepatic gluconeongenesis was suppressed at 48h after sepsis as evaluated in isolated and cultured hepatocytes. Dexamethasone ameliorated in the non-infected liver lobes,but did not in the infected liver lobes. It is concluded that dexamethasone protection in binary sepsis is associated with support of gluconeogenesis, and as a result,amelioration of hypoglycemia.