This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Heusch, G. Articles by Ross, J. Search for Related Content PubMed PubMed Citation Articles by Heusch, G. Articles by Ross, J., Jr

Circulation, Vol 75, 482-490, Copyright © 1987 by American Heart Association

ARTICLES

Attenuation of exercise-induced myocardial ischemia in dogs with recruitment of coronary vasodilator reserve by nifedipine

G Heusch, BD Guth, R Seitelberger and J Ross Jr

There is now evidence that under resting conditions coronary vasodilator reserve exists even in the presence of myocardial ischemia. Therefore, we tested the hypothesis that a vasodilator reserve may exist during exercise so that during exercise-induced ischemia a reduction in coronary constrictor tone can be produced that attenuates the decreases in regional myocardial blood flow and function distal to a severe coronary stenosis without changing the determinants of myocardial oxygen demand. Nine dogs were instrumented with an ameroid constrictor on the left circumflex coronary artery and were studied 2 to 3 weeks later. During a control treadmill run, heart rate increased from 119 +/- 20 to 225 +/- 20 beats/min and peak left ventricular pressure increased from 144 +/- 17 to 163 +/- 28 mm Hg. Poststenotic subendocardial blood flow (measured by a microsphere technique) fell from 1.19 +/- 0.36 to 0.51 +/- 0.30 ml/min X g and systolic wall thickening (by sonomicrometry) decreased from 24.3 +/- 5.8% to 6.0 +/- 6.1%. During an identical run after nifedipine (10 micrograms/kg iv), systemic hemodynamics were not significantly altered. However, subendocardial blood flow was increased to 0.85 +/- 0.51 ml/min X g (p less than .05) and systolic wall thickening to 11.4 +/- 7.8% (p less than .01). We conclude that in this study the amelioration of exercise- induced myocardial ischemia was due to the recruitment by nifedipine of coronary vasodilator reserve.

This article has been cited by other articles:

				D. J. Duncker and R. J. Bache Regulation of Coronary Blood Flow During Exercise Physiol Rev, July 1, 2008; 88(3): 1009 - 1086. [Abstract] [Full Text] [PDF]

				G. Heusch and R. Schulz The role of heart rate and the benefits of heart rate reduction in acute myocardial ischaemia Eur. Heart J. Suppl., September 1, 2007; 9(suppl_F): F8 - F14. [Abstract] [Full Text] [PDF]

				G. Heusch, D. Baumgart, P. Camici, W. Chilian, L. Gregorini, O. Hess, C. Indolfi, and O. Rimoldi {alpha}-Adrenergic Coronary Vasoconstriction and Myocardial Ischemia in Humans Circulation, February 15, 2000; 101(6): 689 - 694. [Abstract] [Full Text] [PDF]

				B. K. Podesser, S. Schwarzacher, W. Zwoelfer, T. M. Binder, E. Wolner, and R. Seitelberger COMPARISON OF PERIOPERATIVE MYOCARDIAL PROTECTION WITH NIFEDIPINE VERSUS NIFEDIPINE AND METOPROLOL IN PATIENTS UNDERGOING ELECTIVE CORONARY ARTERY BYPASS GRAFTING J. Thorac. Cardiovasc. Surg., November 1, 1995; 110(5): 1461 - 1469. [Abstract] [Full Text]

				J. M. Canty Jr and T. P. Smith Jr Adenosine-Recruitable Flow Reserve Is Absent During Myocardial Ischemia in Unanesthetized Dogs Studied in the Basal State Circ. Res., June 1, 1995; 76(6): 1079 - 1087. [Abstract] [Full Text]