Role of cirrhosis in the hemodynamic response to hemorrhage in portal hypertension

Abstract

We studied hemodynamic alterations in normal and three models of portal hypertension at rest, after hemorrhage, and after resuscitation to determine the role of hepatic dysfunction in the splanchnic vascular response to hemorrhage in portal hypertension. One noncirrhotic and two cirrhotic models of portal hypertension were produced in rabbits: partial prehepatic portal vein ligation, common bile duct ligation, and carbon tetrachloride-induced cirrhosis. Animals were subjected to isovolemic hemorrhage followed by reinfusion of shed blood. Portal, central, and aortic pressures, superior mesenteric artery blood flow, and portosystemic shunt were measured. Histologic examination showed parenchymal damage was absent in normal and portal vein ligation, severe in common bile duct ligation, and moderate in carbon tetrachloride-induced cirrhosis. All portal hypertensive animals exhibited diminished splanchnic vasoconstrictive response to hemorrhage compared with normal. The carbon tetrachloride cirrhosis group had severe cirrhotic changes, minimal portosystemic shunt, and mildly diminished constrictive response. In contrast, the portal vein ligation and common bile duct ligation animals had larger portosystemic shunts, markedly diminished constrictive response, and less severe parenchymal damage. A direct correlation existed between magnitude of rise in portal venous pressure or degree of portosystemic shunt and the fall in mesenteric resistance or diminution of vasoconstrictive response to hemorrhage. We concluded that the abnormal splanchnic vascular response in portal hypertension is relatively independent of the degree of hepatic parenchymal injury, but it is related to the degree of portal hypertension and possibly to splanchnic hyperemia.