Figlewicz D P, Filkins J P
Circ Shock. 1978;5(3):317-23.
Dexamethasone acetate (100 microgram IP) protected male Holtzman rats (300-330 gm) against endotoxin shock due to Salmonella enteritidis lipopoly-saccharide B IV. Endotoxin (5.0 mg/rat) produced hypoglycemia within 180 minutes, ie, plasma glucose fell from 87 to 24 mg/dl; dexamethasone prevented the hypoglycemia, ie, plasma glucose levels were 129 mg/dl at 180 minutes after endotoxin. Dexamethasone antagonized both endotoxin-induced depression of hepatic gluconeogenesis and enhanced glucose oxidation as evaluated in vivo. Epididymal fat pads from endotoxic rats (100-110 gm) had increased rates of glucose oxidation as evaluated by the in vitro conversion of 14C-D-glucose to 14CO2. Dexamethasone both in vivo and in vitro antagonized endotoxin glucose hypercatabolism by isolated epididymal fat pads following administrated of endotoxin. Glucocorticoid protection against endotoxin shock is related to antagonism of glucose dyshomeostasis.
醋酸地塞米松（腹腔注射100微克）可保护雄性霍尔兹曼大鼠（体重300 - 330克）免受肠炎沙门氏菌脂多糖B IV所致的内毒素休克。内毒素（5.0毫克/只大鼠）在180分钟内导致低血糖，即血浆葡萄糖从87毫克/分升降至24毫克/分升；地塞米松可预防低血糖，即在内毒素作用180分钟后血浆葡萄糖水平为129毫克/分升。如在体内评估所示，地塞米松可拮抗内毒素诱导的肝糖异生抑制，并增强葡萄糖氧化。通过将14C - D -葡萄糖体外转化为14CO2评估，内毒素血症大鼠（体重100 - 110克）的附睾脂肪垫葡萄糖氧化速率增加。在内毒素给药后，地塞米松在体内和体外均可拮抗附睾脂肪垫分离后的内毒素葡萄糖高分解代谢。糖皮质激素对内毒素休克的保护作用与对葡萄糖稳态失衡的拮抗作用有关。
