Renal and Cerebral Blood Flow in Experimental Liver Failure in the Pig

Abstract

The renal and cerebral blood flow was measured in six pigs after total devascularization of the liver. The animals died 21 to 26 h after the operation, with biochemical and electroencephalographic changes compatible with liver failure. The renal blood flow increased slightly, from 2.12 to 2.61 ml g⁻¹ · min⁻¹, throughout the period of observation but did not differ significantly from that of the controls. Conversely, the cerebral blood flow decreased 38%, from 1.30 to 0.80 ml · g⁻¹ · min⁻¹, p < 0.05. The results failed to confirm a simultaneous decrease in cerebral and renal blood flow due to false neurotransmitters in liver failure, as previously suggested. The results do not support the suggested hypothesis that a substance produced by the liver is essential for renal function and perfusion, nor can they confirm that vasoactive material from the gut is responsible for the renal hypoperfusion in liver failure. The absence of renal hypoperfusion in the present preparation might be due to the exclusion of the failing liver from the circulation, giving indirect evidence to the theory that the vasoactive agent(s) responsible for the renal hypoperfusion in liver failure originates in the failing liver itself.

Key-words:

• Cerebral blood supply
• experimental liver failure
• hepato-renal syndrome
• kidney blood supply
• kidney pathophysiology
• xenon-133 clearance