Lang C H, Molina P E, Skrepnick N, Bagby G J, Spitzer J J
Department of Physiology, Louisiana State University Medical Center, New Orleans 70112.
Am J Physiol. 1994 Jun;266(6 Pt 1):E863-9. doi: 10.1152/ajpendo.1994.266.6.E863.
Previous studies indicate that catecholamines play an important role in mediating the glucose metabolic response to endotoxin. Because acute ethanol (EtOH) intoxication impairs this response, the present study was initiated to ascertain whether EtOH attenuates the lipopolysaccharide response by decreasing the increment in plasma catecholamines after endotoxin or by decreasing the responsiveness of rats to epinephrine. All studies were performed on chronically catheterized fasted rats infused intravenously with either EtOH or an equal volume of saline. In the first series of experiments, intravenous administration of Escherichia coli endotoxin increased, to the same extent, the plasma concentrations of epinephrine and norepinephrine in both saline- and EtOH-infused rats. In the second study, rats were infused with [3-3H]glucose to assess whole body glucose metabolism and the ability of EtOH to alter the glucose metabolic response to epinephrine. The exogenous infusion of a maximally stimulating dose of epinephrine (1 microgram.min-1.kg-1) into saline-infused control animals for 3 h produced a marked hyperglycemia that resulted from a sustained increase in the rate of hepatic glucose production and a reduction in the metabolic clearance rate for glucose. EtOH infusion did not prevent the epinephrine-induced hyperglycemia but blunted the stimulatory effect of epinephrine on glucose production. The differences in glucose metabolism between saline- and EtOH-treated rats could not be explained by changes in plasma insulin or glucagon concentrations. Furthermore, the ability of EtOH to impair the epinephrine-induced increase in glucose production was still evident in rats treated with 4-methylpyrazole, an inhibitor of alcohol dehydrogenase.(ABSTRACT TRUNCATED AT 250 WORDS)
以往的研究表明，儿茶酚胺在介导对内毒素的葡萄糖代谢反应中起重要作用。由于急性乙醇（EtOH）中毒会损害这种反应，因此开展了本研究，以确定EtOH是否通过降低内毒素后血浆儿茶酚胺的增量或降低大鼠对肾上腺素的反应性来减弱脂多糖反应。所有研究均在长期插管的禁食大鼠身上进行，这些大鼠静脉内输注EtOH或等体积的生理盐水。在第一系列实验中，静脉注射大肠杆菌内毒素后，生理盐水输注组和EtOH输注组大鼠的肾上腺素和去甲肾上腺素血浆浓度升高幅度相同。在第二项研究中，给大鼠输注[3-3H]葡萄糖，以评估全身葡萄糖代谢以及EtOH改变对肾上腺素的葡萄糖代谢反应的能力。向生理盐水输注的对照动物中以最大刺激剂量（1微克·分钟-1·千克-1）外源性输注肾上腺素3小时，会产生明显的高血糖，这是由于肝脏葡萄糖生成速率持续增加以及葡萄糖代谢清除率降低所致。EtOH输注并未阻止肾上腺素诱导的高血糖，但减弱了肾上腺素对葡萄糖生成的刺激作用。生理盐水处理组和EtOH处理组大鼠之间的葡萄糖代谢差异无法用血浆胰岛素或胰高血糖素浓度的变化来解释。此外，在用酒精脱氢酶抑制剂4-甲基吡唑处理的大鼠中，EtOH损害肾上腺素诱导的葡萄糖生成增加的能力仍然明显。（摘要截短至250字）
