Effects of Dexmedetomidine Preconditioning on Hepatic Ischemia-Reperfusion Injury in Rats

Dexmedetomidine (Dex), an α2 adrenoceptor selective agonist, has analgesic and sedative effects. Dex preconditioning also can reduce organ damage against ischemia-reperfusion (IR) injury in rat models. We divided the study into two experiments to investigate the protective effects of Dex on hepatic IR injury (IRI) according to dose and the involvement of nitric oxide (NO) in Dex preconditioning, using the NO synthase inhibitor N-nitro-l-arginine methyl ester (L-NAME) and the α2 adrenoceptor blocker atipamezole.

A total of 36 rats were assigned 4 to each group. In the first experiment, the degree of hepatic IR damage was compared at Dex 30, 50, and 70 μg/kg in a hepatic IRI model. In the second experiment, using Dex 50, which showed the most protective effect in the first experiment, serum transaminase, hepatic tissue malondialdehyde levels, hepatic tissue superoxide dismutase activity, and the degree of histopathological assessment were observed in each group using L-NAME and atipamezole, respectively.

Dex preconditioning attenuated hepatic IRI, and the degree of histopathological damage decreased in proportion to the increase in the concentration of Dex. When NO production was inhibited using L-NAME, the histoprotective effect of Dex was reversed; although histopathological hepatic damage increased, biochemical analysis showed that the protective effect of Dex was still remained compared to atipamezol.

Dex preconditioning increased tissue-protective effects against IRI in proportion to the concentration of Dex. Additionally, it is observed that NO plays a partial role in the hepatoprotective effects of Dex compared to α2 adrenoceptor effect.