Hepatic haemodynamics during and after brief occlusion of the hepatic artery

Abstract

Experiments in an instrumented, anaesthetised canine model have: (a) measured the effect of a 5–10 min period of hepatic artery occlusion on hepatic haemodynamics and oxygen consumption ( n = 5); and (b) quantified the post-occlusion reactive hyperaemic responses of the hepatic artery to periods of occlusion ranging from 1 s to 5 min in dogs with interrupted portal blood flow ( n = 5) compared with animals possessing a normal hepatic circulation ( n = 5). (a) Hepatic artery occlusion for 5–10 min produced no significant change in portal venous blood flow or portal vascular resistance. A decrease in total hepatic oxygen consumption (mean, 41%) occurred, which was proportionately greater than the loss of total hepatic blood flow (mean, 33%). (b) Portal flow interruption caused a mean increase in hepatic arterial blood flow of 17.4 ml 100 g −1 per min. The maximum peak hyperaemic response of the hepatic artery after arterial flow occlusion was the same for both groups of dogs studied (34–35 ml 100 g −1 per min), a value achieved following 1 min arterial occlusion in the dogs with intact portal blood supply, and following 4 min arterial occlusion in portally-deprived animals. After a 5 min period of arterial occlusion, there was a 5-fold greater duration of reactive hyperaemia ( P = 0.002) and a 12-fold greater hyperaemic flow volume ( P = 0.049) in the portally-deprived dogs compared with normal dogs. These findings probably reflect a more marked hepatic oxygen debt and accumulation of vasoactive metabolites such as adenosine during hepatic arterial occlusion in the dogs lacking portal blood flow.