Maitra S R, Homan C S, Pan W, Geller E R, Henry M C, Thode H C
Department of Emergency Medicine, UMC, State University of New York, Stony Brook 11794-7400, USA.
Acad Emerg Med. 1996 Nov;3(11):1006-10. doi: 10.1111/j.1553-2712.1996.tb03343.x.
To determine whether endotoxic shock decreases the renal gluconeogenic capacity and the renal artery blood flow.
An in-vivo, murine, nonrecirculating kidney perfusion model was studied in a trauma research laboratory. Each of 12 fasted, male Holtzman rats (shock n = 6, control n = 6) was injected with 1 mL of normal saline or endotoxin (20 mg/kg). Five hours after the injection, all the rats were anesthetized and blood samples were obtained for the determination of the plasma glucose. Right renal artery blood flow was measured by an ultrasonic small-animal flow meter. The kidney was then perfused via the renal artery with 37 degrees C, oxygenated, glucose-free Krebs-Henseleit solution in the presence of 100 mumol of phloridzin to inhibit the cellular uptake of glucose. Renal glucose production was determined by measuring glucose in both renal vein effluent and urine. After 30 minutes of equilibration, 5 mmol of lactate and 0.5 mmol of pyruvate were added to the perfusate as a gluconeogenic substrate. Renal vein and ureteral effluent samples were collected after 5, 10, and 15 minutes.
The endotoxic shock group showed hypoglycemia (p < 0.05) as well as a decrease in renal artery blood flow (p < 0.05). Gluconeogenic stimulation was demonstrable in both the control and the endotoxic shock groups after 15 minutes of perfusion with substrate (p < 0.05). However, renal gluconeogenesis was significantly attenuated in the endotoxic shock group compared with the control.
Renal glucose production in response to a gluconeogenic substrate is significantly attenuated during the hypoglycemic phase of endotoxic shock. Endotoxic shock also causes a significant decrease of renal artery blood flow.
确定内毒素休克是否会降低肾脏糖异生能力和肾动脉血流量。
在创伤研究实验室中研究了一种体内小鼠非循环肾脏灌注模型。12只禁食的雄性霍尔兹曼大鼠（休克组n = 6，对照组n = 6）每只均注射1 mL生理盐水或内毒素（20 mg/kg）。注射后5小时，所有大鼠均被麻醉并采集血样以测定血浆葡萄糖。用超声小动物流量计测量右肾动脉血流量。然后在存在100 μmol根皮苷以抑制细胞摄取葡萄糖的情况下，通过肾动脉用37℃、含氧、无糖的克雷布斯-亨泽莱特溶液灌注肾脏。通过测量肾静脉流出液和尿液中的葡萄糖来确定肾脏葡萄糖生成。平衡30分钟后，向灌注液中添加5 mmol乳酸和0.5 mmol丙酮酸作为糖异生底物。在5、10和15分钟后收集肾静脉和输尿管流出液样本。
内毒素休克组出现低血糖（p < 0.05）以及肾动脉血流量减少（p < 0.05）。在用底物灌注15分钟后，对照组和内毒素休克组均显示出糖异生刺激（p < 0.05）。然而，与对照组相比，内毒素休克组的肾脏糖异生明显减弱。
在内毒素休克的低血糖阶段，对糖异生底物的肾脏葡萄糖生成明显减弱。内毒素休克还会导致肾动脉血流量显著减少。
