Summary
To study the relationship between the disturbance of nitric oxide/endothelin-1 (NO/ET-1) and the hepatic ischemia/reperfusion (I/R) injury as well as the regulation of the NO/ET-1 system by the hepatic ischemic preconditioning (IPC), the changes of the NO/ET-1 system and their relationship with the hepatic I/R injury were compared between the I/R group and the IPC+I/R group in a rat hepatic I/R model. 2 h after reperfusion, the liver tissues were examined for expressed inducible nitric oxide synthase (iNOS) mRNA by RT-PCR. In the acute phase of hepatic reperfusion, the ratio of NO/ET-1 was reduced, which was due to the significant reduction of NO −2 /NO −3 (the metabolic product of NO) and significant elevation of ET-1 in the blood plasma. The content of ALT, AST, LDH and TNF-α in blood plasma, and level of MDA in liver tissue were increased but ATP in liver tissue was reduced, and the hepatic damage was deteriorated. The protection of the hepatic IPC was associated with the elevated ratio of NO/ET-1 caused by the elevation of NO −2 /NO −3 , and reduction of ET-1 as well. No iNOS mRNA was detected in the liver tissues. It was concluded that hepatic I/R injury was related to the disturbance of NO/ET-1. The protection of the hepatic IPC in the acute phase might be mediated by its regulation of NO/ET-1 system. The cNOS rather than the iNOS generated the NO in this scenario.
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References
Cottart C H, Do L, Blanc M Cet al. Hepatoprotective effect of endogenous nitric oxide during Ischemia-Reperfusion in the rat. Hepatology, 1999, 29(3):809
Wang P, Ba Z F, Chaudry I H. Endothelial cell dysfunction occurs very early following trauma-hemorrhage and persists despite fluid resuscitation. Am J Physiol, 1993, 265:H973
Zhang J X, Bauer M, Clemens M G. Vessel-and target cell-specific actions of endothelin-1 and endothelin-3 in rat liver. Am J Physiol, 1995, 269:G269
Lisa M. Colletti, Steven L. Kunkel, Alfred Walz,et al. The role of cytokine networks in the local liver injury following hepatic ischemia/reperfusion in the rat. Hepatology, 1996, 23(3):506
Yoshizumi T, Yanaga K, Soejima Y,et al. Amelioration of liver injury by ischaemic preconditioning. Br J Surg, 1998, 85(12):1636
Peralta C, Hotter G, Closa Det al. The protective role of adenosine in inducing nitric oxide synthesis in rat liver ischemia preconditioning is mediated by activation of adenosine A2 receptors. Hepatology, 1999, 29 (1):126
Gee M H, Albertine K H. Neutrophil-endothelial cell interactions in the lung. Annu Rev Physiol. 1993, 55:227
Yin D P, Sankary H N, Chong A S Fet al. Protective effect of ischemic preconditioning on liver preservation-reperfusion injury in rats. Transplantation, 1998, 66 (2):152
Saavedra J E, Billiar T R, Williams Det al. Targeting nitric oxide (NO) delivery in vivo: design of a liver-selective NO donor prodrug that blocks tumor necrosis factor-α-induced apoptosis and toxicity in the liver. J Med Chem, 1997, 40:1947
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LÜ Ping, male, born in 1968, Doctor in Charge
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Ping, L., Chunyou, W., Daoda, C. et al. The NO/ET-1 system is involved in the protection of the hepatic ischemic preconditioning. Current Medical Science 23, 23–25 (2003). https://doi.org/10.1007/BF02829453
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DOI: https://doi.org/10.1007/BF02829453