The Protection Of Dexmedetomidine Postconditioning Against Ischemia-reperfusion Injury In Isolated Rat Hearts

Background and objective Myocardial ischemia-reperfusion injury is a common, important pathological process in clinical anesthesia, the study of the application of anesthetic in new intervention measures for prevention and treatment of myocardial ischemia-reperfusion injury has become a new hot of research and direction in clinical anesthesia. Dexmedetomidine is a highly selective alpha 2-adrenergic receptor agonists, was used as supplementary drug for the sedation of patients in perioperative period and ICU. The new myocardial protection of dexmedetomidine against ischemia-reperfusion injury was investigated and will have important value and significance in the cardioprotection of anesthetics-induced postconditioning on anti-injury prevention and treatment in clinical anesthesia.Methods Male SD rats were randomly divided into 3 groups: ischemia-reperfusion group(control group), dexmedetomidine 0.23ng/ml group(D I), dexmedetomidine 2.3ng/ml group(D II). Hearts were isolated from rats and perfused with Krebs-Henseleit (K-H) buffer in a Langendorff apparatus. After the end of 15 min equilibration(balance), all hearts were perfused continuously for another 30 min and subjected to 30 min of global no-flow ischemia followed by 120 min of reperfusion. LVEDP, LVDP,+dp/dtmax,-dp/dtmax and HR in the isolated hearts were measured and recorded after 15 min stabilization, before global no-flow ischemia and at reperfusion:R5min, R15min, R30min, R60min, R 90min and R120 min. In addition, the activity of creatine kinase (CK), lactate dehydrogenase (LDH) and myeloperoxidase (MPO) in coronary effluent in the isolated hearts were measured at the end of 15 min equilibration (balance), before global no-flow ischemia, reperfusion immediately and at R 25 min, R 30 min and R 60 min of reperfusion. The infarct size was determined by 2,35-triphenyl tetrazolium chloride(TTC) staining at R 120 min.Results Compared with I/R group, no significant difference was found in cardiac parameters in all groups at the end of 15 min equilibration(balance) and before global no-flow ischemia (P>0.05). Compared with I/R group, HR was reduced significantly in Dâ…  group at R60 min and R90 min of reperfusion (P<0.05); no significant difference was found in LVDP and LVEDP at R 5 min, R15 min, R30 min, R60 min, R90 min and R120 min of reperfusion (P>0.05); +dp/dtmax was reduced significantly at R 60 min, R 90 min and R120 min of reperfusion (P<0.05);-dp/dtmax reduced significantly at R60 min and R90 min of reperfusion (P<0.05). Compared with I/R group, the +dp/dtmax reduced significantly in Dâ…¡ group at R 120 min of reperfusion (P<0.05); no significant difference was found in +dp/dtmax at R5 min, R15 min, R30 min, R 60 min and R 90 min of reperfusion (P<0.05); no significant difference was detected in HR, LVDP, LVEDP and -dp/dtmax at R 5 min, R15 min, R30 min, R60 min, R90 min and R120 min of reperfusion (P>0.05). Compared with I/R group, there was no significant difference in LDH and CK at the end of 15 min equilibration (balance) in all groups before global no-flow ischemia and reperfusion immediately (P>0.05); Compared with I/R group, in D â…  and Dâ…¡ groups, the LDH and CK activity in coronary effluent in the isolated hearts were significantly decreased at R25 min, R60 min and R 90 min of reperfusion (P<0.05); Compared with I/R group, the infarct size was increased in Dâ…  and Dâ…¡ groups (P< 0.05), and there was no significant difference between two groups (P>0.05). Compared with group, MPO activity in coronary effluent in the isolated hearts in Dâ…  and Dâ…¡ group was significantly decreased at 30 min of reperfusion (P<0.05). Conclusion (1) Dexmedetomidine postconditioning can effectively reduce ischemia-reperfusion injury of the isolated rat heart, have a protective effect on rat heart.(2) The protection of dexmedetomidine postconditioning against ischemia-reperfusion injury in isolated rat hearts is related to inhibition of degranulation of cardiac mast cell.