HUMAN AND CANINE VENTRICULAR VASOACTIVE INTESTINAL POLYPEPTIDE - DECREASE WITH HEART-FAILURE

  • 1 July 1986
    • journal article
    • research article
    • Vol. 108  (1) , 11-16
Abstract
Vasoactive intestinal polypeptide (VIP) is a systemic and coronary vasodilator that may have positive inotropic properties. Myocardial levels of VIP were assayed before and after the development of heart failure in two canine models. In the first, cobalt cardiomyopathy was induced in eight dogs; VIP (by radioimmunoassay) decreased from 35 .+-. 11 pg/mg protein (mean .+-. SD) to 5 .+-. 4 pg/mg protein (P < 0.05). In six dogs with doxorubicin-induced heart failure, VIP decreased from 31 .+-. 7 to 11 .+-. 4 pg/mg protein (P < 0.05). In addition, VIP content of left ventricular muscle of resected failing hearts in 10 patients receiving a heart transplant was compared with the papillary muscles in 14 patients (five with rheumatic disease, nine with myxomatous degeneration) receiving mitral valve prostheses. The lowest myocardial VIP concentration was found in the hearts of patients with coronary disease (one patient receiving a transplant and three receiving mitral prostheses) (6.3 .+-. 1.9 pg/mg protein). The other patients undergoing transplantation had an average ejection fraction of 17% .+-. 6% and a VIP level of 8.8 .+-. 3.9 pg/mg protein. The hearts without coronary artery disease (averge ejection fraction of this group 62% .+-. 10%) had a VIP concentration of 14.1 .+-. 7.9 pg/mg protein, and this was greater than in hearts of the patients with coronary disease and the hearts of patients receiving a transplant (P < 0.05). Myocardial catecholamines were also determined in 14 subjects; a weak correlation (r = 0.57, P < 0.05) between the tissue concentrations of VIP and norepinephrine was noted. Reduction of VIP is part of the pathologic process of cardiac failure, but the role of VIP and the mechanism of the reduction remain to be determined.