Abstract
Hepatic venous samples are obtained by introducing a catheter into the liver through the jugular vein (local anesthesia) and portal blood by means of a portal Camilla. Within 2 mins. blood is drawn from the femoral artery and vein and the portal and hepatic veins and analyzed for glucose and lactate. Control detns. indicate that glucose is generally removed by the muscles and viscera and released by the liver. After a 70% hemorrhage (bled out and 30% of the bleeding vol. returned) the avg. maximum glucose portal-hepatic venous difference rises to 10 times the control difference and the glucose arterial-hepatic venous difference to 15 times the control value. This rise in the amt. of glucose released by the liver increases the arterial glucose level in spite of the rise in peripheral glucose utilization (avg. maximum arterial-venous difference 8 times the control value). After reaching these maximum values the portal-hepatic and the arterial-hepatic venous differences decrease until death. In 7 control detns. lactate is generally produced by the muscles and viscera and removed by the liver. During the 1st hr. after a 70% hemorrhage the portal-hepatic venous difference may rise as high as[long dash]20.7 mg. %. However, when this increase in the amt. of lactate removed by the liver occurs, it does not mean that the fraction of the lactate removed (0-29%) is necessarily greater than that removed during the control period (0-48%). As hypoxia continues the ability of the liver to remove the lactate fails progressively and the arterial lactate level rises.

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