[Analysis of liver hemodynamics in severe ischemia and reperfusion injury after liver transplantation].

AIM

The pathogenesis of the ischemia-/reperfusion injury after liver transplantation is not fully understood. The purpose of this study was to analyse blood flow and vascular resistance of the hepatic artery and the portal vein after long ischemic time.

METHODS

A model of orthotopic liver transplantation in pigs was used. Two groups with different cold ischemic times (CIT) were formed: group A: short ischemic time (4-6 hrs CIT), 7 transplantations/group B: long ischemic time (20-24 hrs CIT), 7 transplantations. The blood flow was measured by means of electromagnetic technique. The intravascular pressure was determined in the aorta, portal vein and hepatic vein after direct punction or by inserted catheters.

RESULTS

After short ischemic time and 1 hour of reperfusion a decrease of the arterial and portal venous resistance was observed, while the total hepatic blood flow remained constant. Six hours after reperfusion the arterial and portal venous vascular resistance increased and reached almost values of the donor animal. However, marked changes of hemodynamic parameters were found after long ischemic time, especially in the portal venous vascular system. The vascular resistance of the portal vein was significantly elevated and reached values ten-times higher than during the donor operation.

CONCLUSION

The decrease of the vascular resistance during the early reperfusion period was surprising because of the well-known results of histological studies and analysis of the microcirculation. The cause remained unknown, but an increased perfusion via intrahepatic shunts or denervation of the transplant may be responsible for this observation. The elevated portal venous resistance after severe ischemic damage most likely reflected the increase of interstitial pressure. In the clinic monitoring of the portal venous vascular system by means of doppler-sonography may be an useful adjunct in the diagnosis of early postoperative transplant-dysfunction.