Impact of α-Adrenergic Coronary Vasoconstriction on the Transmural Myocardial Blood Flow Distribution During Humoral and Neuronal Adrenergic Activation

Increased heart rate and left ventricular pressure during humoral and neuronal adrenergic activation act to restrict blood flow preferentially in the subendocardium. The hypothesis was advanced that α-adren-ergic coronary vasoconstriction preferentially in the subepicardium may counterbalance the enhanced extravascular compression in the subendocardium and serve to maintain blood flow transmurally uniform. In 40 anesthetized dogs, regional myocardial blood flow was determined with colored microspheres; wall function, with sonomicrometry. Humoral adrenergic activation (HAA) was induced by a combination of intravenous atropine, intravenous norepinephrine, and atrial pacing during baseline coronary vasomotor tone (group 1, n=6) and in the presence of maximal coronary vasodilation with intravenous dipyridamole (group 2, n=6). In an additional group, HAA was induced by intravenous norepinephrine in the presence of dipyridamole but without atropine and atrial pacing in order to increase end-diastolic left ventricular pressure (group 3, n=6). Measurements were performed at rest, during HAA, and during ongoing HAA with the intracoronary infusion of the α-antagonist phentolamine (Phen). At unchanged mean aortic pressure, Phen improved blood flow particularly to the inner layers as followsfrom 1.42±0.40 (mean±SD) to 1.90±0.40 mL/(ming) (group 1, P