No abstract

Effects of acute portal hypertension on systemic hemodynamics after hepatectomy were evaluated by portal venous stenosis (PVS) model in dogs. In protocol 1, portal hypertension of about twice portal venous pressure (PVP) decreased cardiac output (CO) and left atrial pressure (LAP) by 24.5% (p < 0.01) and 1.0 mm Hg (p < 0.01), respectively. In protocol 2, stepwise PVS demonstrated that CO change (%) and LAP change (mm Hg) were inversely proportional to PVP change (r = -0.937 and -0.883, respectively). The ratio of CO change to LAP change with stepwise PVS was comparable to that obtained by repeated hemorrhage in protocol 3. The present study shows that low CO with portal hypertension is caused by a reduction of venous return to the heart.

The effects of 66 % hepatic congestion (group 2, n = 6) on liver blood flow and hepatic oxygen metabolism were investigated in anesthetized dogs using an ultrasonic transit time flowmeter. The results were compared with those for control dogs (group 1, n = 6) and for 60% hepatectomized dogs (group 3, n = 6) wherein almost the same amount of hepatic parenchyma was removed as was congested in group 2. Portal blood flow (PVF) in group 2 and group 3 decreased similarly to 60 and 63 % of the baseline values, respectively (p < 0.05). Cardiac output (CO) in group 2 and group 3 also decreased significantly in proportion to the decrease in PVF. Among the dogs in group 2, hepatic arterial blood flow (HAF) was fairly well maintained at 86% of the baseline value, despite the decrease of cardiac output, whereas the HAF in group 3 decreased to 49 % of the baseline value at 1 h after hepatectomy. The calculated hepatic arterial resistance (HAR) in group 3 increased significantly due to the 60 % loss of the hepatic arterial vascular bed. The HAR in group 2, by contrast, became lower than that in group 1, suggesting a compensatory decrease of HAR for the obstructed portal flow to the congested area. These results were well consistent with our angiographic findings (n = 3) that the portal flow to the congested segments was completely obstructed and the congested segments received only an arterial blood supply. The centrilobular hepatocytes of the congested segments showed marked vacuolar degeneration and the total hepatic oxygen consumption in group 2 was reduced (p < 0.05). However, the decrease in oxygen consumption in group 2 was not so severe as in group 3 (p < 0.05). These data suggest that some parts of the preserved congested segments were still viable and had the capacity of aerobic metabolism even 4 h after the ligation of the drainage vein of those segments. In this study, the importance of the hepatic arterial flow to the congested segment has been demonstrated. When the congested hepatic segment is to be preserved intraoperatively, care must be taken to maintain the hepatic arterial blood flow during the perioperative period.