We report a model of acute ischemic liver failure which does not require temporary or permanent portal decompression. The model is induced by segmental ischemia of the median and left lateral lobes for 100 min by a vascular clamp applied on the afferent vessels. Declamping is followed by resection of the nonischemic right lateral and caudate lobes. No portal stasis occurs as blood flow to the right lateral and caudate lobes is maintained during the period of clamping. The 24-hour mortality is 76.5%. Evidence of severe liver damage is shown by histological and biochemical studies.

The effects of portal arterialization after portacaval shunt were studied in dogs. Flow- and pressure-adapted portal arterialization was performed by mounting a Teflon cuff on an autogenous vein bypass graft between the hepatic stump of the portal vein and the right renal artery. Immediately following operation, the total hepatic blood flow and intrahepatic portal venous pressure were within normal range. Eight weeks after operation, the intrahepatic portal venous pressure remained within the preoperative range, while total hepatic blood flow had increased double or triple. However, structural change due to increased flow was absent in the liver, even sixteen months after operation. Body weight, liver enzyme chemistry, ICG clearance rate, and amino acid metabolism were well maintained for the entire period of investigation. These findings suggest that sequelae such as hepatic encephalopathy and impaired hepatic metabolism after portacaval shunt can be avoided by portal arterialization, in the presence of an appropriate flow and pressure.

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In the present study, the heat production of liver biopsies (5-8 mg) was measured by a microcalorimetric technique. Tissue incubated in Leibowitz L-15 medium (L-15) showed a higher metabolic rate compared to tissue incubated in a medium without substrate 2.8 microW/mg and 1.75 microW/mg, respectively. Heat production was found to be related to weight density. No difference in the metabolic rate was found after organ perfusion in comparison to nonperfused liver. Storage in medium L-15 at 4 degrees C caused a lower rate of heat production, but if the tissue was stored in an electrolyte balance solution without substrate, no difference was seen compared to fresh tissue. Recording heat production with the present calorimetric technique is relatively simple and rapid and allows measurement of small samples.

Biopsies of ischemic livers demonstrated a significantly higher rate of heat production when incubated in Leibowitz L-15 medium compared to incubation in modified Eagle's solution (P less than 0.01). A maximal reduction of 25% in the rate of heat production was observed after 60 min of induced ischemia. Liver tissue undergoing reperfusion showed complete and partial recovery after 60 and 90 min, respectively. We conclude that the viability of liver tissue begins to deteriorate after 1-1.5 h of ischemia. Using the level of adenosine triphosphate (ATP) as a parameter for viability, others had found this critical time period to be 1.5-2 h. Furthermore, we conclude that monitoring heat production of tissue provides a useful measure of viability for both clinical application and in connection with experimental liver surgery.