IMPACT OF ALPHA-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 preferential ly in the subendocardium. The hypothesis was advanced that alpha-adren ergic coronary vasoconstriction preferentially in the subepicardium ma y counterbalance the enhanced extravascular compression in the subendo cardium and serve to maintain blood flow transmurally uniform. In 40 a nesthetized dogs, regional myocardial blood flow was determined with c olored microspheres; wall function, with sonomicrometry. Humoral adren ergic activation (HAA) was induced by a combination of intravenous atr opine, intravenous norepinephrine, and atrial pacing during baseline c oronary 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 pacin g 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 alpha-antagonist p hentolamine (Phen). At unchanged mean aortic pressure, Phen improved b lood flow particularly to the inner layers as follows: from 1.42 +/- 0 .40 (mean +/- SD) to 1.90 +/- 0.40 mL/(min.g) (group 1, P < .05), from 4.99 +/- 2.31 to 5.53 +/- 2.56 mL/(min.g) (group 2, P < .05), and fro m 6.01 +/- 1.41 to 6.29 +/- 1.27 mL/(min.g) (group 3, P < .05), associ ated with a decrease in outer layer blood flow in groups 2 and 3. In 1 6 additional dogs, beta-adrenoceptors were blocked by propranolol and muscarinic receptors by atropine. Neuronal adrenergic activation (NAA) was induced by cardiac sympathetic nerve stimulation (CSNS) during ba seline coronary vasomotor tone (group 4, n = 8) and in the presence of maximal vasodilation (group 5, n = 8). Measurements were performed at rest, during a first CSNS, and 20 minutes later during a second CSNS + Phen. The reproducibility of two consecutive episodes of CSNS 20 min utes apart was demonstrated in a separate set of experiments (n = 6). At matched mean aortic pressures, Phen improved blood flow to all myoc ardial layers in group 4, whereas in group 5, Phen induced a redistrib ution of myocardial blood flow toward subepicardial layers [from 4.44 +/- 0.96 to 4.81 +/- 0.83 mL/(min.g), P < .05] at the expense of inner layers. With the addition of Phen, there was no change in regional wa ll function in any group of dogs studied. Thus, during HAA, alpha-adre nergic coronary vasoconstriction does not exert a beneficial effect on transmural blood flow distribution. During NAA, a beneficial effect o f a-adrenergic coronary vasoconstriction becomes apparent only under c onditions of maximal coronary vasodilation.