Abstract
The physiological regulation of the liver blood flow is a result of a reciprocal portal vein and hepatic artery flow relationship. This mechanism is defined as the hepatic arterial buffer response (HABR). This study was addressed to investigate whether HABR is maintained in denervated grafts in liver transplant recipients. Portal blood flow (PBF) and hepatic arterial resistance index (PI) were measured 6 months after transplantation using Doppler. In each patient we consecutively measured the vasodilator (Ensure Plus PO versus placebo) and vasoconstrictor (isosorbide dinitrate 5 mg SL versus placebo) stimuli. The meal ingestion caused a significant increase of both parameters, PBF (from 1495±260 to 2069±250 mL/min, P<0.05) and PI (from 0.7±0.2 to 0.8±0.2, P<0.05). By contrast, isosorbide dinitrate reduced PBF (from 1660±270 to 1397±250 mL/min, P<0.05) and PI (from 0.7±0.2 to 0.5±0.2, P<0.05). We show that PBF and PI are reciprocally modified with the administration of vasoconstrictor and vasodilator stimuli. These results suggest the persistence of the HABR in a denervated human model, suggesting that this mechanism is independent of the regulation from the autonomic nervous system.
Highlights
Portal hypertension is associated with systemic hyperdynamic state characterized by a high cardiac output and a low peripheral vascular resistance [1]
It has been suggested that hepatic artery plays a passive role; that is, fluctuations in portal blood flow are buffered by inverse changes in arterial flow [6,7,8]
Systemic and hepatic hemodynamic parameters were evaluated in eight patients with cirrhosis after six months of liver transplantation
Summary
Portal hypertension is associated with systemic hyperdynamic state characterized by a high cardiac output and a low peripheral vascular resistance [1]. Several experimental and clinical evidences have demonstrated reciprocity between changes in blood flow in the hepatic artery and the portal vein. It has been suggested that hepatic artery plays a passive role; that is, fluctuations in portal blood flow are buffered by inverse changes in arterial flow [6,7,8]. Until now, this physiological relationship has not been evaluated in stable liver transplant recipients. The aims of the present study were (a) to evaluate hepatic arterial and portal blood flows after liver transplantation and (b) to measure the response of the hepatic artery to portal flow variations
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