Effect of Ethanol on Hepatic Oxygenation: Evidence of Hepatic Hypoxia
It is well established that oxygen is required for the metabolism of ethanol in the liver and that hepatic oxygen consumption is stimulated by acute or chronic administration of ethanol. Our recent study in the perfused liver clearly demonstrated a vasoconstrictive effect of ethanol in the presinusoidal region, which led to hepatic tissue hypoxia due to a reduction in oxygen supply to hepatocytes (Hijioka et al., 1988). This evidence suggests that ethanol could damage the liver via mechanisms involving tissue hypoxia. However, a recent study in baboons has revealed an impaired hepatic oxygen utilization after large doses of ethanol (40–70mM) (Lieber et al., 1989). The mechanism may be a direct toxic effect of ethanol on oxygen utilization in mitochondria, possibly via accumulation of aldehyde, or by a microcirculatory disturbance which reduces delivery of oxygen to the regional hepatic tissue. We have determined the sinusoidal blood hemoglobin oxygenation using a sensitive spectrophotometer, coupled with an in vivo microscope, and demonstrated a clear oxygenation gradient in the sinusoidal blood from periportal to pericentral regions. Ethanol exaggerated this oxygen gradient (Sato et al., 1987). The purpose of the present study is to evaluate the effect of ethanol on hepatic oxygenation by means of that spectrophotometric method and also a Polarographic method and thereby to clarify whether ethanol produces hepatic hypoxia.
KeywordsHepatic Tissue Hepatic Blood Flow Hepatic Lobule Pericentral Region Ethanol Administration
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