|
|
||||||||
Ann Thorac Surg 1997;63:1050-1056
© 1997 The Society of Thoracic Surgeons
Department of Cardiovascular Surgery, Montreal Heart Institute, Montreal, Quebec, Canada
Accepted for publication October 30, 1996.
Background. Calcium-channel blockers have been reported to improve myocardial recovery after ischemia-reperfusion, but their effects on coronary blood flow regulation remain to be defined. Experiments were designed to evaluate the effects of calcium antagonists on coronary artery vasoregulation exposed to ischemia-reperfusion.
Methods. Three groups of hearts (n = 6) were pretreated with a 10-minute infusion of either diltiazem, verapamil, or nifedipine at concentrations of 10-9 mol/L to 10-6 mol/L and exposed to 30 minutes of no-flow ischemia and 45 minutes of reperfusion. Another group (n = 6) received no pretreatment and was used as control. Endothelium-dependent and -independent relaxations were tested by assessing coronary flow increase to 5-hydroxytryptamine (10-6 mol/L) and sodium nitroprusside (10-5 mol/L) infusion, respectively. Left ventricular pressure, its first derivative, and coronary basal flow were recorded before and after ischemia as well as during calcium antagonist infusion.
Results. Endothelium-dependent relaxation after ischemia was significantly improved with all three drugs in a dose-dependent fashion; nifedipine was found to be the more potent. Endothelium-independent relaxation was also significantly preserved with calcium antagonists regardless of the type, whereas left ventricular hemodynamics were not. During perfusion, nifedipine was found to have the most negative inotropic effect and to be the most potent vasodilator on the coronary circulation. Diltiazem was the less effective drug on both left ventricular hemodynamics and coronary circulation.
Conclusions. This study indicates that preischemic infusion of calcium antagonists enhance endothelium-dependent and -independent coronary artery relaxation in the isolated rat heart model in a dose- and drug-dependent fashion. This can be achieved at low doses without affecting left ventricular hemodynamics and should contribute to preserve coronary artery autoregulation.
This article has been cited by other articles:
![]() |
D. Lopez, A. Rodriguez-Sinovas, L. Agullo, J. Inserte, A. Cabestrero, and D. Garcia-Dorado Acidic reoxygenation protects against endothelial dysfunction in rat aortic rings submitted to simulated ischemia Am J Physiol Heart Circ Physiol, December 1, 2008; 295(6): H2409 - H2416. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. K. S. Camara, Q. Chen, S. S. Rhodes, M. L. Riess, and D. F. Stowe Negative inotropic drugs alter indexes of cytosolic [Ca2+]-left ventricular pressure relationships after ischemia Am J Physiol Heart Circ Physiol, August 1, 2004; 287(2): H667 - H680. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Schafer, S. Walther, M. Schafer, L. Dieterich, S. Kasseckert, Y. Abdallah, and H.M. Piper Inhibition of contractile activation reduces reoxygenation-induced endothelial gap formation Cardiovasc Res, April 1, 2003; 58(1): 149 - 155. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Ladilov, C. Schafer, A. Held, M. Schafer, T. Noll, and H.M. Piper Mechanism of Ca2+ overload in endothelial cells exposed to simulated ischemia Cardiovasc Res, August 1, 2000; 47(2): 394 - 403. [Abstract] [Full Text] [PDF] |
||||
![]() |
P P. Dimitrow, M Krzanowski, R Nizankowski, A Szczeklik, and J S Dubiel Effect of verapamil on systolic and diastolic coronary blood flow velocity in asymptomatic and mildly symptomatic patients with hypertrophic cardiomyopathy Heart, March 1, 2000; 83(3): 262 - 266. [Abstract] [Full Text] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |