HEPATIC HEMODYNAMICS DURING AND AFTER BRIEF OCCLUSION OF THE HEPATIC-ARTERY

Experiments in an instrumented, anaesthetised canine model have: (a) m easured the effect of a 5-10 min period of hepatic artery occlusion on hepatic haemodynamics and oxygen consumption (n = 5): and (b) quantif ied the post-occlusion reactive hyperaemic responses of the hepatic ar tery to periods of occlusion ranging from 1 s to 5 min in dogs with in terrupted 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 consum ption (mean, 41%) occurred, which was proportionately greater than the loss of total hepatic blood flow (mean, 33%). (b) Portal flow interru ption 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 hepati c 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 hyp eraemic flow volume (P = 0.049) in the portally-deprived does compared with normal dogs. These findings probably reflect a more marked hepat ic oxygen debt and accumulation of vasoactive metabolites such as aden osine during hepatic arterial occlusion in the dogs lacking portal blo od flow. (C) 1997 Elsevier Science Ireland Ltd.