Protective effects of Dex on myocardial injury induced by hepatic cold ischemia reperfusion

Objective To explore the effects of dexmedetomidine on myocardial injury during liver cold ischemia reperfusion in rats. Methods A total of 40 healthy male Sprague-Dawley (SD)rats with a weight of 220~250 gram and an age of 8~10 weeks were randomly divided into 5 groups of sham, model, Dex, Atip and AG490 by a random number table (n=8 each). At 8h post-reperfusion, blood samples were harvested from infra-hepatic vena cava and serum levels of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), creatine kinase-muscle/brain (CK-MB), troponin I (cTnI)and heart-type fatty acid binding protein (H-FABP)determined by enzyme-linked immunosorbent assay (ELISA). After blood sampling, the rats were sacrificed, the expression of activated caspase-3 was detected by immunohistochemistry and apoptotic cells by TUNEL.Apoptotic rate was calculated.And the phosphorylations of JAK2, STAT1 and STAT3 were assessed by Western blot. Results As compared with sham group, the levels of TNF-α, IL-6, CK-MB, cTnI and H-FABP significantly increased, apoptotic rate spiked, pathological damage worsened and the expressions of activated caspase-3, p-JAK2, p-STAT1 and p-STAT3 were up-regulated in other groups (P<0.05); As compared with model group, the levels of TNF-α, IL-6, CK-MB, cTnI and H-FABP significantly decreased, apoptotic rate declined, pathological damage became alleviated and the expressions of activated caspase-3, p-JAK2, p-STAT1 and p-STAT3 became down-regulated in groups Dex and AG490 (P<0.05); as compared with group Dex, the levels of TNF-α, IL-6, CK-MB, cTnI and H-FABP significantly increased, apoptotic rate rose, pathological damage worsened and the expressions of activated caspase-3, p-JAK2, p-STAT1 and p-STAT3 became up-regulated in group Atip (P<0.05). Conclusions Dexmedetomidine can ameliorate myocardial injury induced by liver cold ischemia-reperfusion in rats. Key words: Liver; Reperfusion injury; Myocardium; Apoptosis