The preventative role of growth hormone on acute liver injury induced by cardiopulmonary bypass in a rat model

Objective: Cardiopulmonary bypass (CPB)-induced acute liver injury is a life-threatening complication after cardiac surgery and is thought to be associated with inflammatory response and acute-phase response (APR). Recombinant human growth hormone (rhGH) can modulate the APR and inflammatory response. Here, we tested the protective effect of GH on CPB-induced liver injury in the rat. Methods: Adult mate Sprague Dawley rats (group G, received 2.5 mg/kg of rhGH intramuscularly at 8 a.m. every 24 h for 3 days and just before the initiation of CPB; group C served as control) under-went CPB (120 min, 120 ml/kg per minute, 34 degrees C) and were killed 3 h after the termination of CPB. Results: Administration of rhGH markedly increased serum insulin-like growth factor (IGF)-I and IGF-I-binding protein (IGFBP)-3 compared with group C. Group G showed significantly tower serum concentrations of alanine aminotransferase and total bilirubin after CPB termination. Those receiving rhGH demonstrated a significant increase in serum prealbumin and serum transferrin and a marked decrease in serum amyloid A and serum C-reactive protein compared with group C. rhGH significantly decreased serum tumor necrosis factor-alpha (TNF-alpha) and interteukin-1 beta (IL-1 beta), whereas no changes were found for serum IL-6 and IL-10 compared with group C. rhGH significantly increased total liver protein content, hepatocyte proliferation, and decreased hepatocyte apoptosis versus group C. Conclusions: These results suggest that GH administration in rats seems to play a preventative role in acute liver injury associated with CPB via the decrease in acute-phase proteins, proinflammatory cytokines TNF-alpha and IL-1 beta, and hepatocyte apoptosis, which is associated with increase in constitutive hepatic proteins, total liver protein content, and hepatocyte proliferation. (C) 2007 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved.