AIM: Dexmedetomidine is a highly selective α-2 adrenergic agonist used perioperatively. Dexmedetomidine's cardioprotective effect after myocardial ischaemia remains unknown. In this study, we administered dexmedetomidine after ischaemia to investigate its ability to protect the cardiac muscle from ischaemia-reperfusion injury in isolated rat hearts. METHODS: After a 30-min stop of perfusion, isolated rat hearts underwent reperfusion for 120 min. At the initiation of reperfusion, dexmedetomidine was administered for 25 min at concentrations of 0 nM (control group), 1 nM (Dex 1 group), and 10 nM (Dex 10 group). Yohimbine (an α-2 adrenergic antagonist) was administered in the manner as above in another group of isolated rat hearts at a concentration of 1 μM without dexmedetomidine (Yoh group) and at 1 μM with 10 nM dexmedetomidine (Yoh+Dex 10 group). The area of infarction was measured using 2,3,5-triphenyltetrazolium staining. RESULTS: Dexmedetomidine administration did not influence haemodynamics or the coronary flow (CF), but did increase the myocardial infarct size. Neither concentration of dexmedetomidine affected the infarct size as the Dex 1 and Dex 10 groups had almost the same infarct size. The infarct size was 40.5±2.9% in the control group, 60.9±5.3% in the Dex 1 group, and 60.9±2.8% in the Dex 10 group. The infarct size was reduced in the yohimbine groups. The infarct size was 39.2±3.3% in the Yoh+Dex 10 group and 45.0±3.2% in the Yoh group. CONCLUSION: Dexmedetomidine administration does not influence haemodynamics or CF, but does increase the cardiac infarct size. α-2 Adrenergic stimulation may induce this mechanism.
AIM: Dexmedetomidine is a highly selective α-2 adrenergic agonist used perioperatively. Dexmedetomidine's cardioprotective effect after myocardial ischaemia remains unknown. In this study, we administered dexmedetomidine after ischaemia to investigate its ability to protect the cardiac muscle from ischaemia-reperfusion injury in isolated rat hearts. METHODS: After a 30-min stop of perfusion, isolated rat hearts underwent reperfusion for 120 min. At the initiation of reperfusion, dexmedetomidine was administered for 25 min at concentrations of 0 nM (control group), 1 nM (Dex 1 group), and 10 nM (Dex 10 group). Yohimbine (an α-2 adrenergic antagonist) was administered in the manner as above in another group of isolated rat hearts at a concentration of 1 μM without dexmedetomidine (Yoh group) and at 1 μM with 10 nM dexmedetomidine (Yoh+Dex 10 group). The area of infarction was measured using 2,3,5-triphenyltetrazolium staining. RESULTS:Dexmedetomidine administration did not influence haemodynamics or the coronary flow (CF), but did increase the myocardial infarct size. Neither concentration of dexmedetomidine affected the infarct size as the Dex 1 and Dex 10 groups had almost the same infarct size. The infarct size was 40.5±2.9% in the control group, 60.9±5.3% in the Dex 1 group, and 60.9±2.8% in the Dex 10 group. The infarct size was reduced in the yohimbine groups. The infarct size was 39.2±3.3% in the Yoh+Dex 10 group and 45.0±3.2% in the Yoh group. CONCLUSION:Dexmedetomidine administration does not influence haemodynamics or CF, but does increase the cardiac infarct size. α-2 Adrenergic stimulation may induce this mechanism.
Authors: Ke Peng; Wei-Rong Chen; Fan Xia; Hong Liu; Xiao-Wen Meng; Juan Zhang; Hua-Yue Liu; Zheng-Yuan Xia; Fu-Hai Ji Journal: J Cell Mol Med Date: 2019-11-03 Impact factor: 5.310