Reilly F D, McCafferty R E, Cilento E V
Department of Anatomy, School of Medicine, West Virginia University, Morgantown 26506.
Microcirc Endothelium Lymphatics. 1988 Aug;4(4):293-309.
Circulating-blood glucose, hepatic glycogen distribution, and the glycogen contents of liver and skeletal muscle, were determined for 60 min in 31 fed and anesthetized Sprague-Dawley rats. These rats received an endoportal infusion of 15 mg per kg b.w. E. coli endotoxin (026:B6) or of sterile saline solution as a control. Either substance was given intravenously at 9:30 a.m. following an intraperitoneal injection at 9:00 a.m. of 0.1 mg per kg b.w. prazosin or 0.3 mg per kg b.w. yohimbine or of the carrier, distilled water. Infused endotoxin elevated blood glucose without affecting hepatic glycogen distribution and total glycogen contents of liver and skeletal muscle when compared to control. Prazosin inhibited endotoxin-induced hyperglycemia, and prazosin plus endotoxin provoked centrilobular glycogen depletion and decreased total hepatic glycogen content. However, no significant alteration in the glycogen content of skeletal muscle accompanied blockade of glucogenesis. Prazosin administered by itself produced no changes in hepatic and muscle glycogen. Although yohimbine blocked endotoxin-induced hyperglycemia, yohimbine, or yohimbine plus endotoxin, produced no significant change in the glycogen contents of liver and skeletal muscle. Blockade in the latter case was associated with some depletion of glycogen in hepatocytes dispersed randomly throughout the unit lobule and in cells located centrivenously. These results suggested that endotoxin-induced hyperglycemia is evoked by activation of alpha-1 and -2 adrenergic receptors. Since no detectible change in hepatic glycogen distribution and in the contents of liver and muscle glycogen accompanied glucogenesis, glycogen catabolism and deposition are postulated to proceed simultaneously and at equivalent rates by 60 min following the experimental induction of endotoxemia. Blockade of alpha (one or two) adrenoceptors is hypothesized to inhibit endotoxin-induced hyperglycemia by facilitating glucose utilization and not by stimulating glycogenesis or by antagonizing glycogenolysis in the liver or skeletal muscle.
对31只喂食后麻醉的Sprague-Dawley大鼠在60分钟内测定了循环血糖、肝糖原分布以及肝脏和骨骼肌的糖原含量。这些大鼠接受了每千克体重15毫克大肠杆菌内毒素（026:B6）的门静脉内输注或无菌盐溶液作为对照。在上午9:00腹腔注射每千克体重0.1毫克哌唑嗪或每千克体重0.3毫克育亨宾或载体蒸馏水后，于上午9:30静脉注射上述两种物质中的一种。与对照组相比，输注内毒素可升高血糖，但不影响肝糖原分布以及肝脏和骨骼肌的总糖原含量。哌唑嗪可抑制内毒素诱导的高血糖，哌唑嗪加内毒素可引起小叶中心糖原耗竭并降低肝脏总糖原含量。然而，糖原异生受阻时骨骼肌糖原含量无明显变化。单独给予哌唑嗪对肝脏和肌肉糖原无影响。尽管育亨宾可阻断内毒素诱导的高血糖，但育亨宾或育亨宾加内毒素对肝脏和骨骼肌的糖原含量无明显影响。在后一种情况下的阻断与整个单位小叶随机分布的肝细胞以及小叶中心部位细胞中的糖原部分耗竭有关。这些结果表明，内毒素诱导的高血糖是由α-1和-2肾上腺素能受体激活引起的。由于在内毒素血症实验诱导后60分钟，肝糖原分布以及肝脏和肌肉糖原含量没有可检测到的变化，因此推测糖原分解代谢和沉积同时进行且速率相当。假设阻断α（一或二）肾上腺素能受体可通过促进葡萄糖利用而非刺激糖原合成或拮抗肝脏或骨骼肌中的糖原分解来抑制内毒素诱导的高血糖。
