Impaired endothelium-dependent relaxation of human hepatic arteries after preservation with the University of Wisconsin solution.

Abstract

To evaluate the effect of University of Wisconsin solution on endothelium-dependent relaxation and contraction of human hepatic arteries in vitro. Human hepatic arteries were harvested from 24 patients with hepatocellular carcinoma who had undergone hepatectomy. A tertiary care center. Human hepatic arteries (n = 6 in each group) were harvested during resection for hepatocellular carcinoma. The arteries in group 1 (i.e., the control group) were immediately studied without preservation. The arteries in group 2 were preserved in cold (4 degrees C) physiological solution for 1 hour, while the arteries in groups 3 and 4 were preserved in University of Wisconsin solution for 1 and 16 hours, respectively. Segments of control and preserved hepatic arteries with or without endothelium were then suspended in organ chambers to measure the isometric force. The relaxation of segments of the hepatic arteries with endothelium in response to acetylcholine and adenosine diphosphate was significantly (P < .05) greater than that of segments without endothelium. The maximal relaxation of hepatic arterial segments with endothelium in groups 3 and 4 in response to acetylcholine was notably different from that of segments in groups 1 and 2. The maximal relaxation of hepatic arterial segments with endothelium in groups 3 and 4 in response to adenosine diphosphate was notably different from that of segments in groups 1 and 2. Perfusate hypoxia (mean +/- SD PO2, 30 +/- 5 mm Hg) caused the endothelium-dependent contraction of the arteries (the median initial tension in groups 1, 2, 3, and 4 was 251%, 233%, 276%, and 260%, respectively; P > .05). The endothelium-dependent relaxation of human hepatic arteries in response to acetylcholine and adenosine diphosphate was notably attenuated by University of Wisconsin solution. The impaired endothelium-dependent relaxation by University of Wisconsin solution and the prominent endothelium-dependent contraction of human hepatic arteries would favor vasospasm and thrombosis after hepatic transplantation.