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

Dose-related responses to acetylcholine, adenosine 5'-triphosphate (ATP), a denosine and sodium nitroprusside were studied in an in vitro perfused rabb it liver gassed with (95% N-2/5% CO2, 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 Grou p 1 and responses to all but sodium nitroprusside were abolished in Group 2 . Portal venous responses to acetylcholine, adenosine and sodium nitropruss ide were not significantly altered in either Group 1 or Group 2. However, p ortal venous vasoconstriction to ATP was significantly enhanced in Group 1 and less so in Group 2. It is concluded that carbon dioxide-free hypoxia at tenuated hepatic arterial vasodilatation to acetylcholine and ATP and enhan ced vasonstriction to ATP. Both these effects may be characteristic of dama ge to the microvascular endothelium and may be the result of decreased synt hesis of nitric oxide. (C) 1999 Elsevier Science B.V. All rights reserved.