Effect of propofol on endothelin-1 and nitric oxide during hepatic ischemia-reperfusion injury in rabbits

Objective: To investigate the effect of propofol on endothelin-1 (ET-1) and nitric oxide (NO) during hepatic ischemia-reperfusion injury (HIRI) in rabbits in vivo and to investigate its protective effect on HIRI. Methods: A total of 40 rabbits were randomly divided into four groups with ten animals in each. They were ischemia-reperfusion group (group A), ischemia-reperfusion group treated with 2 ml_/(kg · h) sodium chloride (group B), ischemia-reperfusion group treated with 8 mg/(kg · h) propofol (group C), and sham-operation group as control (group D). ET-1 and NO content in hepatic tissue and serum, and alanine aminotransferase (ALT), aspartate aminotransferase (AST) content in serum were assayed 30 and 60 min after reperfusion. Morphological observation of hepatic tissues was also performed. Results: In groups A, B, and C 30 and 60 min after reperfusion, ET-1 content in hepatic tissue and serum increased compared with that in group D (P < 0.01 or P<0.05), but the increased degree in group C was much smaller than that in group A and B at the same time (P< 0.01). NO content in hepatic tissue and serum decreased compared with that of group D (P<0.01 or P<0. 05), but the decreased degree in group C was much smaller than that in group A and B at the same time (P<0. 01). Serum ALT and AST level in group A, B, and C increased compared with that in group D (P<0.01 or P<0.05), but the increased degree in group C was much smaller than that in group A and B at the same time (P<0.01). The morphology of hepatocytes changed abnormally. The blood stasis of hepatic tissue in group C was milder than that in group A and B, denaturalization and necrosis of hepatocyte in group C were not obvious. Conclusion: Propofol can protect hepatic sinus endothelium, decrease ET-1 content and increase NO content, and thus it shows the protective effect on HIRI.