Acute impairment of endothelium-dependent relaxations to aggregating platelets following reperfusion injury in canine coronary arteries

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Circulation Research. 1990;67:385-393

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ARTICLES

Acute impairment of endothelium-dependent relaxations to aggregating platelets following reperfusion injury in canine coronary arteries

PJ Pearson, HV Schaff and PM Vanhoutte
Department of Physiology and Biophysics, Mayo Clinic, Rochester, Minn.

Experiments were designed to determine whether endothelial injury contributes to augmented coronary vascular tone seen during myocardial reperfusion. Canine left anterior descending coronary arteries were exposed to ischemia followed by reperfusion (60 minutes each). Rings (3- 4 mm) of the reperfused artery and of normal left circumflex (control) coronary artery segments were prepared. Rings were suspended for isometric force measurement in organ chambers containing modified Krebs' Ringer bicarbonate solution (37 degrees C, 95% O2-5% CO2). Endothelium-independent contractions to KCl and prostaglandin F2 alpha were unaltered after reperfusion. Endothelium-dependent relaxations to nitric oxide, sodium nitroprusside, and isoproterenol were comparable in control and reperfused arteries. However, reperfused coronary arteries contracted with prostaglandin F2 alpha lost the ability to express endothelium-dependent relaxations to aggregating platelets. Reperfused arterial rings also exhibited impaired endothelium-dependent relaxations to acetylcholine, the calcium ionophore A23187, and the platelet-derived compounds ADP and serotonin. Quiescent (noncontracted) reperfused arterial rings exhibited larger contractions than controls when exposed to aggregating platelets. In such quiescent rings, the endothelium-dependent increase in tension to hemoglobin was unaltered after reperfusion. Thus, coronary reperfusion impairs the normal endothelium-dependent relaxations to aggregating platelets and vasoactive drugs. This impairment of platelet-mediated coronary relaxation could help explain the increased vascular tone and tendency toward vasospasm commonly observed after reperfusion of the coronary arteries.

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				A. W. Wallace and W. L. Tom Interaction of L-Arginine and Phosphodiesterase Inhibitors in Vasodilation of the Porcine Internal Mammary Artery Anesth. Analg., April 1, 2000; 90(4): 840 - 846. [Abstract] [Full Text] [PDF]

				J.-F. Bouchard, J. Chouinard, and D. Lamontagne Participation of prostaglandin E2 in the endothelial protective effect of ischaemic preconditioning in isolated rat heart Cardiovasc Res, January 14, 2000; 45(2): 418 - 427. [Abstract] [Full Text] [PDF]

				L. P Perrault, J.-P. Bidouard, P. Janiak, N. Villeneuve, P. Bruneval, J.-P. Vilaine, and P. M Vanhoutte Impairment of G-protein-mediated signal transduction in the porcine coronary endothelium during rejection after heart transplantation Cardiovasc Res, August 1, 1999; 43(2): 457 - 470. [Abstract] [Full Text] [PDF]

				S. P. Marrelli, A. Khorovets, T. D. Johnson, W. F. Childres, and R. M. Bryan Jr. P2 purinoceptor-mediated dilations in the rat middle cerebral artery after ischemia-reperfusion Am J Physiol Heart Circ Physiol, January 1, 1999; 276(1): H33 - H41. [Abstract] [Full Text] [PDF]

				M. Carrier, M. Pellerin, P. L. Page, N. R. Searle, R. Martineau, C. Caron, B. C. Solymoss, and L. C. Pelletier Can L-arginine improve myocardial protection during cardioplegic arrest? Results of a phase I pilot study Ann. Thorac. Surg., July 1, 1998; 66(1): 108 - 112. [Abstract] [Full Text] [PDF]

				J.-F. Bouchard and D. Lamontagne Protection afforded by preconditioning to the diabetic heart against ischaemic injury Cardiovasc Res, January 1, 1998; 37(1): 82 - 90. [Abstract] [Full Text] [PDF]

				N. Kaeffer, V. Richard, and C. Thuillez Delayed Coronary Endothelial Protection 24 Hours After Preconditioning : Role of Free Radicals Circulation, October 7, 1997; 96(7): 2311 - 2316. [Abstract] [Full Text]

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				B.C. Yang, W.W. Nichols, and J.L. Mehta Cardioprotective Effects of Red Blood Cells on Ischemia and Reperfusion Injury in Isolated Rat Heart: Release of Nitric Oxide as a Potential Mechanism Journal of Cardiovascular Pharmacology and Therapeutics, October 1, 1996; 1(4): 297 - 306. [Abstract] [PDF]

				J. F. Seccombe and H. V. Schaff Coronary Artery Endothelial Function After Myocardial Ischemia and Reperfusion Ann. Thorac. Surg., September 1, 1995; 60(3): 778 - 788. [Abstract] [Full Text]

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