AIM To study the effects of dexmedetomidine combined with remote ischemic preconditioning on myocardial ischemia reperfusion injury and to evaluate its effect on apoptosis.
METHODS Eighty patients scheduled for heart valve replacement under cardiopulmonary bypass were randomly divided into 4 groups (n = 20): a control group (group C), a limb ischemia preconditioning group (group R), a dexmedetomidine pretreatment group (group D), and a dexmedetomidine pretreatment combined with limb ischemia preconditioning group (group DR). Group R received upper limb ischemic preconditioning after induction of anesthesia. In group D, dexmedetomidine was intravenously administered as a loading dose of 11 μg/kg for 10 min and then intravenously 0.41 μg/(kg·h) until the completion of the operation. Plasma troponin I (cTnI) levels were measured before aortic occlusion (T0), at the end of cardiopulmonary bypass (T1) and after the operation (T2). The contents of Bcl-2 and Bax protein and cardiomyocyte apoptosis index (AI) were measured before aortic occlusion and at the end of cardiopulmonary bypass.
RESULTS Compared with group C, at T1 and T2, plasma cTnI decreased in all the other groups (P < 0. 05). Compared with those before aortic clamping, Bcl-2, Bax protein content and AI in the cardiac tissues of the four groups increased, and Bcl-2/Bax decreased after CPB (P < 0.05). Compared with those in group C, the protein of Bcl-2 and Bcl-2/Bax increased and the protein of Bax and AI decreased in group D, group R and group DR (P < 0.05). Compared with those in group R and D, the content of Bcl-2 and Bcl-2/Bax protein in the DR group increased and the value of Bax protein and AI decreased (P < 0.05).
CONCLUSION Dexmedetomidine and limb remote ischemic preconditioning reduce myocardial ischemia reperfusion injury and the combined effects of the two are superior when compared to individual results. Inhibition of cell apoptosis is likely mechanisticly involved.
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