Archer L T, Benjamin B, Lane M M, Hinshaw L B
Am J Physiol. 1976 Sep;231(3):872-9. doi: 10.1152/ajplegacy.1976.231.3.872.
The roles of renal gluconeogenesis and glucose utilization in control, hemorrhaged, and endotoxin-injected animals were investigated using anesthetized, eviscerated, nonnephrectomized and nephrectomized dogs. Results demonstrate an increased glucose utilization in both hemorrhagic and endotoxic shock which was marked after endotoxin. Since blood glucose values dropped more in nephrectomized, hemorrhaged animals, in contrast to the nonnephrectomized, hemorrhaged dogs, the kidneys were assumed to perform a significant gluconeogenic role. The kidneys did not appear to perform gluconeogenesis in endotoxin shock since blood glucose levels were comparable in eviscerated, endotoxin-treated animals whether nephrectomized or not. To ascertain the tissue responsible for the increased glucose utilization in endotoxin shock, a study was performed with endotoxin added to blood in vitro (estimated LD100 concentration). The endotoxin-treated blood (n = 7) demonstrated an increased glucose utilization compared with saline controls (n = 7) (P less than or equal 0.02). Acclerated glucose utilization rates were comparable between the eviscerated, nephrectomized animals and in vitro experiments. These data suggest that excessive glucose demand by certain blood components may partially explain the lethal hypoglycemia of endotoxin shock.
利用麻醉、去内脏、未切除肾脏和切除肾脏的犬，研究了肾脏糖异生和葡萄糖利用在对照动物、出血动物和注射内毒素动物中的作用。结果表明，在出血性休克和内毒素性休克中葡萄糖利用均增加，在内毒素作用后更为明显。由于与未切除肾脏的出血犬相比，切除肾脏的出血动物血糖值下降更多，因此推测肾脏具有重要的糖异生作用。在内毒素休克中，肾脏似乎不进行糖异生，因为无论是否切除肾脏，去内脏并经内毒素处理的动物血糖水平相当。为了确定在内毒素休克中导致葡萄糖利用增加的组织，进行了一项体外研究，向血液中添加内毒素（估计的半数致死剂量浓度）。与生理盐水对照组（n = 7）相比，经内毒素处理的血液（n = 7）显示葡萄糖利用增加（P≤0.02）。去内脏、切除肾脏的动物的葡萄糖利用率加速与体外实验相当。这些数据表明，某些血液成分对葡萄糖的过度需求可能部分解释了内毒素休克致死性低血糖的原因。
