Regional myocardial blood flow during nicotine infusion after chronic coronary artery occlusion: effect of beta-adrenergic blockade.

In eight dogs a portion of the left ventricular free wall (LVFW) was rendered collateral-dependent (CD) by gradual occlusion of the left anterior descending coronary artery with a surgically implanted Ameroid constrictor. Six to 8 weeks later, the dogs were anesthetized and regional myocardial blood flow was measured with 7-10-micron radioactive microspheres during (a) control conditions, (b) nicotine alone (24 micrograms/kg/min i.v.), and (c) nicotine (24 micrograms/kg/min i.v.) after beta-adrenergic blockade with propranolol. During control conditions, mean transmural flow was similar in CD, border, and normal regions of the LVFW. Nicotine alone increased flow in all regions of the LVFW, with normal (+ 104%) greater than CD (+ 56%). These changes in flow were accompanied by increases in mean arterial pressure (+ 34%) and mean aortic flow (+ 54%). Nicotine after beta-adrenergic blockade appreciably raised mean arterial pressure (+ 83%) and mean left atrial pressure (+ 307%), but caused no increase in flow to any region of the LVFW. The results indicate (a) that the nicotine-induced increase in flow is blunted in a CD region, and that (b) beta-adrenergic blockade unmasks coronary vasoconstrictor mechanisms during nicotine infusion which prevent increases in flow to either normal or CD regions despite increased perfusion pressure and augmented myocardial oxygen demands.