The role of adenosine in the hyperaemic response of the hepatic artery to portal vein occlusion (the ‘buffer response’)

Abstract

Adenosine has been shown to be responsible for the hyperaemic response of the hepatic artery to portal vein occlusion (the hepatic arterial 'buffer response'). 2 The effect of adenosine receptor blockade and of adenosine uptake inhibition on the hepatic arterial response to portal vein occlusion was investigated in three groups of anaesthetized dogs. 3 Venous return and arterial blood pressure were maintained during periods of portal occlusion by establishing a side-to-side portacaval shunt. Hepatic artery and portal vein blood flows were measured with electromagnetic flowmeters.4 Hepatic arterial infusions of 8-phenyltheophylline (500pgkg-1 min-1) and 3-isobutyl-1-methylxanthine (75pgkg-min-1), doses sufficient to block the vasodilator response of the hepatic artery to exogenously applied adenosine, reduced the magnitude of the 'buffer response' by 50% and 75%, respectively.

H2S contributes to the hepatic arterial buffer response and mediates vasorelaxation of the hepatic artery via activation of KATP channels

“…Mathie et al (16) postulated that PV provides the major blood supply of oxygen to the liver and that its loss could lead to a certain degree of hepatic hypoxia. In line with the present observation that HABR could not fully compensate for reduced PV inflow, hepatic tissue oxygenation was found reduced during SMA occlusion but still in the physiological range of liver tissue PO 2 (21,27).…”

“…HABR is specific to the unique vascular bed of the liver and is apparently regulated by adenosine (5,10,13,16,27).…”

Nitric oxide is the mediator of ATP‐induced dilatation of the rabbit hepatic arterial vascular bed

“…The importance of adenosine in the control of hepatic arterial (HA) blood flow has recently been established Ezzat & Lautt, 1987;Mathie & Alexander, 1990), and a regulatory role for adenosine 5'-triphosphate (ATP) has also been suggested (Mathie & Alexander, 1990). Work from our laboratory has demonstrated, in the HA vascular bed of the rabbit, the existence of purinoceptors which mediate adenosine-induced vasodilatation (A2 receptors; Mathie et al, 1991), and ATP-induced vasoconstriction (P2X receptors) and vasodilatation (P2Y receptors) (Ralevic et al, 1991a).…”

Ultrasonographic evaluation of abdominal organs after cardiac surgery

“…This way, excessive irregular changes in total hepatic blood flow are prevented, and total oxygen delivery to the liver is maintained irrespective of reductions or enhancements in portal venous oxygen supply [30,31]. This hepatic arterial buffer response is partially mediated by the release of adenosine from the liver [32,33]. Specifically, adenosine is released locally around terminal hepatic arterioles and hepatic venules, whereas its concentration is regulated by flow through a "washout" effect as follows: when portal flow increases, more adenosine is washed out leading to hepatic arterial constriction and a decrease in the hepatic arterial flow.…”