This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Maturi, M. F. Articles by Green, M. V. Search for Related Content PubMed PubMed Citation Articles by Maturi, M. F. Articles by Green, M. V.

Circulation, Vol 83, 2111-2121, Copyright © 1991 by American Heart Association

ARTICLES

Coronary vasoconstriction induced by vasopressin. Production of myocardial ischemia in dogs by constriction of nondiseased small vessels

MF Maturi, SE Martin, D Markle, M Maxwell, CR Burruss, E Speir, R Greene, YM Ro, D Vitale and MV Green
Experimental Physiology and Pharmacology Section, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md.

BACKGROUND. We studied the effect of intracoronary administration of arginine-8-vasopressin on blood flow in nondiseased coronary arteries and determined whether this vasoconstriction was severe enough to produce ischemia in 30 dogs. METHODS AND RESULTS. In group 1 (n = 6), after vasopressin administration coronary blood flow was decreased by 41% (p less than 0.002) without changes in heart rate or aortic pressure, and left ventricular ejection fraction measured by radionuclide angiocardiography was decreased by 18% (p less than 0.0005). In group 2 (n = 6), ischemia was confirmed by measurement of transmural pH changes. Administration of vasopressin decreased subendocardial pH of the infused zone from 7.40 +/- 0.03 to 7.31 +/- 0.07 (p less than 0.01). The subendocardial pH of the zone not infused with vasopressin did not change. To overcome the intrinsic regulation of blood flow, operating primarily in small coronary arteries, we hypothesized that vasopressin must increase resistance primarily in large rather than small coronary arteries. After intracoronary infusion in group 3 (n = 6), however, most (94%) of the increase in resistance during vasopressin administration was explained by an increase of resistance in small coronary arteries. In group 4 (n = 9), vasopressin decreased coronary blood flow by 50% and decreased local shortening by 90% at a time when systemic hemodynamics were unchanged. Coronary constriction induced by vasopressin, or the recovery from it, also was not altered by cyclooxygenase blockade. CONCLUSIONS. Thus, vasopressin produces myocardial ischemia by constricting small, nondiseased coronary arteries severely enough to overcome the competition from normal coronary regulation, and this ischemic event is not mediated by prostaglandin products.

This article has been cited by other articles:

				R. M. Hays Vasopressin Antagonists -- Progress and Promise N. Engl. J. Med., November 16, 2006; 355(20): 2146 - 2148. [Full Text] [PDF]

				W. Wei, C.-Q. Yang, A. Furnary, and G.-W. He Greater vasopressin-induced vasoconstriction and inferior effects of nitrovasodilators and milrinone in the radial artery than in the internal thoracic artery J. Thorac. Cardiovasc. Surg., January 1, 2005; 129(1): 33 - 40. [Abstract] [Full Text] [PDF]

				W. Wei, H. S. Floten, and G.-W. He Interaction between vasodilators and vasopressin in internal mammary artery and clinical significance Ann. Thorac. Surg., February 1, 2002; 73(2): 516 - 522. [Abstract] [Full Text] [PDF]

				H. Hupf, D. Grimm, G. A. J. Riegger, and H. Schunkert Evidence for a Vasopressin System in the Rat Heart Circ. Res., February 19, 1999; 84(3): 365 - 370. [Abstract] [Full Text] [PDF]