Cardioprotective effect of dexmedetomidine for prevention of neurogenic myocardial dystrophy in cardiac and non-cardiac surgical patients

Dexmedetomidine demonstrates cardioprotective effects for various non-cardiac surgical procedures, including those on the aorta, vessels, and hip joint. A significant aspect of the mechanism of dexmedetomidine as an α₂-adrenoceptor agonist involves its sympatholytic effect. The observed effects of dexmedetomidine are associated with its ability to stabilize hemodynamics and reduce the incidence of intraoperative myocardial ischemia. Experimental and clinical evidence has demonstrated that sympatholytic drugs, such as ganglion blockers in doses that block sympathetic ganglia, sympatholytics, and epidural anesthetics, have a cardioprotective effect by preventing the sympathetic dysregulation of trophic processes in the myocardium. Dystrophic changes in the myocardium, induced by the experimental irritation of the reflexogenic area of the aortic arch in rats and rabbits, were prevented by the prior administration of ganglion blockers and sympatholytics. The similar effects were observed in clinical trials with cardiac surgical patients who received epidural anesthetics, which also have a sympatholytic effect. The cardioprotective effect of dexmedetomidine is associated with the prevention of intraoperative neurogenic (reflex) myocardial dystrophy. This effect is achieved by inhibiting the irritation of the reflexogenic areas during periods of sympathoadrenal overactivation, thereby preventing the myocardial depletion of the neurotransmitter noradrenaline and the onset of neurogenic (reflex) dystrophic changes.