Primary graft dysfunction following orthoptic liver transplantation has been ascribed to thrombotic and ischemic complications in a high proportion of cases. It has been suggested that hypothermic storage of livers in preservation solutions elicits damage to the vascular endothelium. Since the endothelium controls vasoactivity and hemostasis via release of endothelium derived relaxing factor (EDRF) and prostacyclin (PGI2), storage injury to the endothelium may predispose the allograft to thrombosis, ischemia and impaired perfusion. In order to test this, the effect of long-term hypothermic storage in modified University of Wisconsin solution (UW), kidney perfusion solution (KPS) and minimum essential medium (MEM) on phenylephrine (PE)-stimulated contraction and acetylcholine (ACh)-stimulated relaxation, as well as PGI2 release by rabbit aortic rings was investigated. Following cold storage for 24, 48 and 72 h, PE and ACh dose response curves were unaffected by storage in MEM, UW or KPS. Following hypothermic storage for 24 h and 48 h, PGI2 release (stimulated with PE, ACh, arachidonate, fluoride, calcium ionophore and phorbol ester) was not significantly altered from zero time responses. These results demonstrate that hypothermic storage of rabbit aortic rings in both UW and KPS do not influence two key endothelial functions (the release of EDRF or PGI2) which in turn indicates that endothelial damage associated with reperfusion following hypothermic storage is not causally related to alterations in EDRF and PGI2 release.