DIRECT CORONARY VASODILATION INDUCED BY INTRACORONARY VASOACTIVE-INTESTINAL-PEPTIDE

Vasoactive intestinal peptide (VIP) is a neurotransmitter that has been identified in epicardial coronary arteries. To evaluate the direct effect of VIP on coronary hemodynamics and blood flow, graded doses of VIP (0.01, 0.03, 0.10, and 0.30 μg/min) were infused into the left coronary artery of 7 patients at the time of diagnostic cardiac catheterization for chest pain syndromes. None of the patients had coronary stenoses >50% during subsequent angiography. Coronary sinus VIP concentrations increased during each infusion (22 ± 28 pg/ml at baseline to 109 ± 22 pg/ml at 0.30 μg/min; p < 0.05), but arterial VIP was elevated (39 ± 29 pg/ml) only at the maximal dose of 0.30 μg/min. During all dosages of VIP, heart rate, right atrial and left ventricular end-diastolic pressure, and the heart rate × blood pressure product did not change. Moreover, neither mean aortic pressure nor left ventricular peak + dP/dt changed significantly at doses <0.30 μg/min; at 0.30 μg/min, mean aortic pressure decreased (97 ± 15 to 90 ± 15 mm Hg; p < 0.05) and LV peak + dP/dt increased (1,621 ± 230 to 1,801 ± 226 mm Hg/s; p < 0.05). Compared to baseline, the arterial-coronary sinus O2 content difference and myocardial O2 extraction diminished progressively at the 0.03, 0.10, and 0.30 μg/min doses of VIP (118 ± 12 ml O2/L vs. 94 ± 15, 70 ± 9, and 61 ± 26 ml O2/L, respectively, and 0.64 ± 0.05 vs. 0.53 ± 0.10, 0.38 ± 0.06, and 0.34 ± 0.15, respectively). In the absence of hemodynamic alterations indicating a substantial variation in myocardial oxygen demand, these changes imply an increase in coronary blood flow and confirm that VIP has a direct effect on the coronary vasculature. These data support the concept that VIP may have a physiological role in the regulation of coronary resistance in man. © 1990 Raven Press, Ltd., New York.