The effect of α1-adrenergic blockade with prazosin on myocardial blood flow at rest and during two levels of treadmill exercise was assessed in 16 chronically instrumented dogs 9-14 days after myocardial infarction had been produced by occlusion of the left circumflex coronary artery. During resting conditions prazosin did not alter mean myocardial blood flow or the subendocardial-to-subepicardial flow ratio in either normally perfused or collateral-dependent myocardium. However, during exercise at comparable external work loads and comparable rate-pressure products, prazosin significantly increased blood flow to normally perfused (27% increase at the second level of exercise, P < 0.001) and collateral-dependent myocardium (35% increase at the second level of exercise, P < 0.001) compared with control. In addition, prazosin caused a small but significant decrease in the subendocardial-to-subepicardial flow ratio in both normal (1.27 ± 0.04 to 1.19 ± 0.04; P < 0.01) and collateral-dependent myocardium (0.57 ± 0.11 to 0.52 ± 0.11; P < 0.01) compared with control, reflecting a disproportionally greater increase in subepicardial flow in response to α1-adrenergic blockade. These data demonstrate that α1-adrenergic vasoconstriction inhibits coronary vasodilation during exercise, even in areas of collateral-dependent myocardium relatively early after coronary artery occlusion.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||2 30-2|
|State||Published - 1991|
- Collateral-dependent myocardium
- Coronary vasoconstriction