Alterations in intrahepatic hemodynamics of the harvested porcine liver

Hemodynamic properties of a donor liver, during initial reperfusion, are as sociated with the degree of graft preservation injury and have been propose d to correlate with subsequent markers of liver function. In the present st udy, hepatic hemodynamics, that is, portal venous pressure, hepatic vascula r resistance, and compliance (vascular distensibility), were characterized (1) in situ before porcine livers were manipulated, (2) after these same li vers were isolated and perfused within a bypass circuit, and (3) on reperfu sion after 2 hours of cold ischemia. Hepatic vascular resistance was determ ined in each of these three states from the portal vein pressure response t o differing hepatic blood flows. In addition, the response of the same live rs to norepinephrine and nitroprusside was evaluated in each condition. In the in situ and isolated perfused liver, portal venous pressure increased o nly modestly despite doubling of hepatic flows. After cold ischemia, the pr essure response to higher flows was significantly greater and much less of a reduction in hepatic vascular resistance was noted than in studies prior to cold ischemia. Unlike livers prior to cold ischemia, the pressure respon se to norepinephrine was attenuated following cold ischemia. The response t o nitroprusside, however, remained intact reducing the portal pressure to t hat of in situ livers. Therefore the portal hypertension that follows cold ischemia appears to be largely provoked by the preservation injury and not by surgical manipulation or the by, pass circuit. This increment in portal pressure is responsive to a nitric oxide donor.