Hypoxia attenuates hepatic arterial vasodilatation and enhances portal venous vasoconstriction to ATP in the perfused rabbit liver

Abstract

Dose-related responses to acetylcholine, adenosine 5′-triphosphate (ATP), adenosine and sodium nitroprusside were studied in an in vitro perfused rabbit liver gassed with (95% N 2/5% CO 2, Group 1) and without carbon dioxide (100% N 2, Group 2). At raised tone, achieved by addition of methoxamine to the perfusate, significantly attenuated hepatic arterial vasodilatation to sodium nitroprusside, acetylcholine, ATP and adenosine was measured in Group 1 and responses to all but sodium nitroprusside were abolished in Group 2. Portal venous responses to acetylcholine, adenosine and sodium nitroprusside were not significantly altered in either Group 1 or Group 2. However, portal venous vasoconstriction to ATP was significantly enhanced in Group 1 and less so in Group 2. It is concluded that carbon dioxide-free hypoxia attenuated hepatic arterial vasodilatation to acetylcholine and ATP and enhanced vasonstriction to ATP. Both these effects may be characteristic of damage to the microvascular endothelium and may be the result of decreased synthesis of nitric oxide.