Coronary vascular effects of dexmedetomidine during reactive hyperemia in the anesthetized dog

The central sympatholytic effects of alpha2-adrenergic agonists are believed to be beneficial during myocardial ischemia, but the peripheral vasoconstrictive effects are controversial. The aim of this study was to investigate the coronary vascular effects of dexmedetomidine (DM) during reactive hyperemia. The study had a prospective, randomized, open-comparative design. University animal laboratory. Nine mongrel dogs. Coronary artery occlusions lasting 2 minutes were induced five times at 40-minute intervals. DM, 0.1, 1, and 10 μg/kg was administered 15 minutes before the second, third, and fourth coronary occlusion, respectively. The alpha2-antagonist atipamezole was administered before the fifth coronary occlusion. DM, 1 μg/kg, significantly decreased heart rate (from 128 ± 13 to 96 ± 21 beats/min); 10 μg/kg of DM also significantly decreased cardiac output (from 3.4 ± 1.1 to 1.4 ± 0.4 L/min). DM decreased myocardial blood flow in all layers of normally perfused myocardium. In hyperemic myocardium, DM significantly decreased epicardial blood flow (from 3.30 ± 1.43 to 1.44 ± 0.49 mL/min/g after DM 10 μg/kg), whereas endocardial blood flow did not change, hereby significantly increasing the endo / epi blood flow ratio (from 0.99 ± 0.54 to 2.28 ± 0.78). In the postischemic hyperemic subendocardial layer, coronary blood flow was preserved after DM. DM reduced primary determinants of myocardial oxygen demand. These effects of DM may be beneficial in conditions of temporary coronary artery occlusion and subsequent reperfusion.