[The protective effect of the limb ischemia preconditioning on the hepatic injury related to NO/ET-1 system in rats].

Objective: To study the relationship between the disturbance of nitric oxide/endothelin-I (NO/ET-1) and the hepatic injury following limb ischemia/reperfusion (I/R) in rats as well as the regulation of NO/ET-1 system by limb ischemia preconditioning (IPC).

Methods: Using limb ischemia/reperfusion injury model rats, animals were randomly divided into three groups (n = 6): control group, I/R group and IPC group. The contents of alanine aminotransferase (ALT), aspartate aminotransferase (AST) in the plasma as well as nitric oxide (NO), endothelin-1 (ET-1), nitric oxide/endothelin-1 (NO/ET-1) in the plasma and the liver were measured. The levels of total nitric oxide synthase (tNOS), inducible nitric oxide synthase (iNOS), constitutive nitric oxide synthase (cNOS) in the liver were determined. The expression of iNOS and endothelial NOS (eNOS) were detected by the immunohistochemical method. The morphologic changes stained with hematoxylineosin were observed under microscope.

Results: It was found that the levels of NO, ET-1 in the plasma and the liver tissue all increased after reperfusion, while the values of ALT, AST, NO/ET-1 decreased. Liver pathology revealed that after limb I/R there were edema, villous microvascular congestion, infiltration of polymorphonuclear neutrophil (PMN), cell degeneration in part cells of the liver. The hepatic damage was deteriorated. While the expression of iNOS elevated, cNOS (mainly eNOS) reduced and total NOS increased. The protection of the limb IPC attenuated the disturbance of NO/ET-1.

Conclusion: The hepatic injury following limb I/R is related to the disturbance of NO/ ET-1. The protection of the limb IPC might be conducted by its regulation of NO/ET-1 system. The elevation of endothelial NOS and the reduction of non-endothelial NOS generated the NO in this situation.