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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 radio-immunoassay) 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
falling 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 election fraction of 17% ± 6% and a VIP
level of 8.8 ± 3.9 pg/mg protein. The hearts without coronary artery disease (average
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.
Abbreviations:
%ΔD (percent change in systole of left ventricular minor axis dimension), dP/dt max (maximum rate of rise in ventricular pressure), VIP (vasoactive intestinal polypeptide)To read this article in full you will need to make a payment
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Article info
Publication history
Accepted:
March 18,
1986
Received:
August 9,
1985
Footnotes
☆Supported in part by the Central Ohio Heart Chapter of the American Heart Association and by the Samuel J. Roessler Research Foundation.
Identification
Copyright
© 1986 Published by Elsevier Inc.
