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Aspects of hepatic hypoxia: observations on the isolated, perfused pig liver.

T HE liver represents only 2% of the body mass and consumes about 25% of the total resting oxygen uptake. Yet hypoxia is not considered to be a significant cause of clinical liver damage. This may be either because hypoxic liver damage is difficult to detect or because the human liver is relatively resistant to hypoxia. Reduction of the hepatic oxygen supply to about so% by clamping the hepatic artery' was not found to reduce the hepatic oxygen uptake in man, but the oxygen tension of the hepatic venous blood became so low (about 20 mm. Hg) that further reduction in supply presumably is incompatible with normal oxidative metabolism. Also, reduction of the hepatic inflow via the portal vein by means of vasopressin failed to affect hepatic oxygen uptake.2 There is little doubt, however, that physiologic regulatory mechanisms exist. Thus, a sojourn at high altitude (3,550 m.) was accompanied by a significant rise in splanchnic blood flow as determined by an indirect method.3 The era of transplantation has renewed interest in the effect of hypoxia on the liver because the transport of the liver from the donor to the recipient inevitably involves a period of anoxia which may determine the viability of the organ.4 The isolated, perfused liver offers good opportunities to study the metabolic effects of hypoxia more closely because the supply of oxygen can be predetermined