H Cao1, Z Wu, X Zhang, H Zhang, Z Chen, Y Kuang. 1. Department of Surgery, Ren Ji Hospital, Shanghai Second Medical University, Shanghai 200001, China.
Abstract
OBJECTIVE: To investigate early changes in systemic and splanchnic hemodynamics after orthotopic liver transplantation (OLT) in normal and cirrhotic rats. METHODS: Male Sprague-Dawley rats were divided into 4 groups: normal controls (NL, n = 10), intrahepatic portal hypertension (IHPH, n = 10) induced by injection of CCl4, normal rats with OLT (NL-OLT, n = 9) and IHPH rats with OLT (IHPH-OLT, n = 16). IHPH-OLT rats were divided into 2 subgroups: 3 days (Group A, n = 9) and 7 days (Group B, n = 7) after OLT. OLT was performed in rats using cuffs for the anastomosis of the suprahepatic inferior vena cava, infrahepatic vena cava and portal vein. Two weeks after production of IHPH rats, 7 days after NL-OLT rats, 3 days and 7 days after IHPH-OLT rats, radioactive microspheres were used in a hemodynamic study. RESULTS: There were no significant differences in hemodynamic changes between NL-OLT and NL rats, except mean arterial blood pressure (MAP). The characteristics of systemic and splanchnic hyperdynamic circulatory state, including increased cardiac output and splanchnic blood flow, decreased mean arterial blood pressure, total peripheral vascular resistance and splanchnic vascular resistance were observed in IHPH, IHPH-OLT A, and IHPH-OLT B rats. The magnitude of hyperhemodynamics was in the order of IHPH > IHPH-OLT A > IHPH-OLT B rats. Moreover, the derangement of splanchnic hyperhemodynamics was more significant than that of systemic hyperthermodynamics. CONCLUSIONS: The present study demonstrates that the persistence of early systemic and splanchnic hyperkinetic circulation after OLT may be the consequence of factors which maintain hyperhemodynamics in liver cirrhosis, where portal hypertension is not completely eliminated. Hyperhemodynamics is not induced by OLT per se.
OBJECTIVE: To investigate early changes in systemic and splanchnic hemodynamics after orthotopic liver transplantation (OLT) in normal and cirrhotic rats. METHODS: Male Sprague-Dawley rats were divided into 4 groups: normal controls (NL, n = 10), intrahepatic portal hypertension (IHPH, n = 10) induced by injection of CCl4, normal rats with OLT (NL-OLT, n = 9) and IHPH rats with OLT (IHPH-OLT, n = 16). IHPH-OLT rats were divided into 2 subgroups: 3 days (Group A, n = 9) and 7 days (Group B, n = 7) after OLT. OLT was performed in rats using cuffs for the anastomosis of the suprahepatic inferior vena cava, infrahepatic vena cava and portal vein. Two weeks after production of IHPH rats, 7 days after NL-OLT rats, 3 days and 7 days after IHPH-OLT rats, radioactive microspheres were used in a hemodynamic study. RESULTS: There were no significant differences in hemodynamic changes between NL-OLT and NL rats, except mean arterial blood pressure (MAP). The characteristics of systemic and splanchnic hyperdynamic circulatory state, including increased cardiac output and splanchnic blood flow, decreased mean arterial blood pressure, total peripheral vascular resistance and splanchnic vascular resistance were observed in IHPH, IHPH-OLT A, and IHPH-OLT B rats. The magnitude of hyperhemodynamics was in the order of IHPH > IHPH-OLT A > IHPH-OLT B rats. Moreover, the derangement of splanchnic hyperhemodynamics was more significant than that of systemic hyperthermodynamics. CONCLUSIONS: The present study demonstrates that the persistence of early systemic and splanchnic hyperkinetic circulation after OLT may be the consequence of factors which maintain hyperhemodynamics in liver cirrhosis, where portal hypertension is not completely eliminated. Hyperhemodynamics is not induced by OLT per se.