Abstract

Using graded flow rates through a passive portalsystemic bypass during 2-hr portal occlusion in dogs, splanchnic, hemodynamic, and metabolic changes and liver insults were evaluated to determine critical bypass flow. To exclude effects caused by reduced circulating blood volume, constant preocclusion levels of cardiac output were maintained throughout the study by increasing intravenous infusion rates. With the decrease in bypass flow rates during portal occlusion, portal pressure increased, superior mesenteric arterial flow decreased, and hepatic arterial flow rapidly increased and these parameters maintained their individual levels during occlusion. These hemodynamic parameters recovered to nearly normal levels 3 hr after release of the portal clamp. Metabolic acidosis progressed with decreasing bypass flow, but portal potassium and inorganic phosphorus levels showed a significant rise only when there was no bypass. Portal levels of creatine phosphokinase BB, β-glucuronidase, and endotoxin did not show significant changes corresponding to bypass flow. The amounts of infusion required were 3 to 6 times the basal level (10 ml/kg/hr) during occlusion and 1.7 to 3 times after release in 30% or less bypass groups. Upon ceasing infusion 3 hr after release, dogs in the 10% or less bypass groups underwent circulatory insufficiency. Changes in total adenine nucleotide and energy charge ratio of the liver, postoperative changes in transaminase levels, and animal survival indicated that a 2-hr interruption of the portal flow, either sufficiently or insufficiently bypassed, caused only minimal insults of the liver. In conclusion, a bypass flow of 30% or more is the critical level for dogs to survive 2 hr of portal occlusion without adverse consequences.

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