Effect of Autoperfusion of the Liver on Detoxication of Thiopental Sodium

¹ From the Department of Physiology and Banting and Best Department of Medical Research, University of Toronto, Toronto, Canada

A decrease in hepatic circulation in dogs causes a significant delay in the detoxication of thiopental sodium. A method has been devised for arterial or venous autoperfusion of the liver with blood from the dog's own vascular system through an extracorporeal circuit driven by a pump with positive action valves. This produces an increase in flow even in damaged livers. In normal dogs the fall of plasma levels of thiopental is accelerated by autoprefusion of the liver. In Eck fistula dogs the retarded detoxication of thiopental became normal again after arterial autoperfusion. In Eck fistula dogs with subsequent (30 hr.) ligation of the common hepatic artery, the decreased rate of detoxication of thiopental is restored to normal by arterial or venous autoperfusion of the liver 18 hours after the ligation. The rate of detoxication of thiopental sodium depends not only on the state of the hepatic parenchyma, but also, to a surprising degree, on the amount of blood flowing through the liver. The clinical use of hepatic arterial autoperfusion is suggested in severe thiopental sodium (Pentothal) poisoning not responding to the usual therapy.