McKaigney J P, Carmichael F J, Saldivia V, Israel Y, Orrego H
Am J Physiol. 1986 Apr;250(4 Pt 1):G518-23. doi: 10.1152/ajpgi.1986.250.4.G518.
In this study we report the effect on splanchnic hemodynamics of acute oral ethanol at doses ranging from 0.25 to 4.0 g/kg body wt. Flows were determined by use of a radioactive microsphere technique. Ethanol was found to increase portal blood flow by 23-57%. In awake rats this increase reached a plateau at the 0.5 g/kg dose. In ketamine-anesthetized rats, the increase was observed only at doses of 3.0 g/kg or more, with the response at doses of 0.5, 1.0, and 2.0 g/kg being suppressed by ketamine. Inhibition of alcohol dehydrogenase by intra-arterial administration of 4-methylpyrazole resulted in suppression of the liver blood flow increase after ethanol was administered to awake animals. Ethanol in the range of doses studied did not result in changes in blood glucagon levels. Rats fed ethanol-containing diets for 4 wk and withdrawn for 18 h had the same response to acute oral ethanol as did naive rats. It is suggested that ethanol metabolism mediates the effects of ethanol on splanchnic blood flow. An increase in splanchnic blood flow when concurrent with an increase in liver O2 consumption induced by ethanol might protect the liver from hypoxic damage.
在本研究中，我们报告了剂量范围为0.25至4.0克/千克体重的急性口服乙醇对内脏血流动力学的影响。血流通过放射性微球技术测定。发现乙醇可使门静脉血流量增加23%至57%。在清醒大鼠中，这种增加在0.5克/千克剂量时达到平台期。在氯胺酮麻醉的大鼠中，仅在3.0克/千克或更高剂量时观察到增加，而在0.5、1.0和2.0克/千克剂量时的反应被氯胺酮抑制。通过动脉内给予4-甲基吡唑抑制乙醇脱氢酶，导致向清醒动物给予乙醇后肝脏血流量增加受到抑制。在所研究的剂量范围内，乙醇不会导致血液中胰高血糖素水平的变化。喂食含乙醇饮食4周并戒断18小时的大鼠对急性口服乙醇的反应与未接触过乙醇的大鼠相同。提示乙醇代谢介导了乙醇对内脏血流的影响。当内脏血流量增加与乙醇诱导的肝脏耗氧量增加同时发生时，可能会保护肝脏免受缺氧损伤。
