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 Mc Fadden, E. P. Articles by Bertrand, M. E. Search for Related Content PubMed PubMed Citation Articles by Mc Fadden, E. P. Articles by Bertrand, M. E.

Circulation, Vol 88, 2076-2085, Copyright © 1993 by American Heart Association

ARTICLES

Response of human coronary arteries to serotonin after injury by coronary angioplasty

EP Mc Fadden, C Bauters, JM Lablanche, P Quandalle, F Leroy and ME Bertrand
Service de Cardiologie B et Hemodynamique, Hopital Cardiologique, Lille, France.

BACKGROUND. Atherosclerotic stenoses that have exaggerated vasomotor responses are especially prone to restenosis after coronary angioplasty. Experimental studies show that vasomotor responses in normal vessels are altered by acute mechanical injury, an alteration that in part reflects changes in the functional characteristics of endothelium that has regenerated after injury. METHODS AND RESULTS. We examined, by quantitative coronary arteriography, the response of dilated and control coronary segments to intracoronary infusions of graded doses of serotonin, an endothelium-dependent vasoactive agent, and to intracoronary injection of isosorbide dinitrate, an endothelium- independent smooth muscle dilator in 15 patients who had undergone a single percutaneous transluminal coronary angioplasty procedure and who had no clinical features of variant angina. Dose-dependent constriction to serotonin occurred at all measured sites. The mean +/- SEM diameter reductions, expressed as percent reduction in baseline diameter that was observed at proximal (18.1 +/- 2.9, 18.8 +/- 2.2) and distal (30.9 +/- 4.4, 35.4 +/- 5.3) control sites in the dilated and nondilated vessels, respectively, at the highest dose, were similar. The degree of constriction in distal segments was significantly (P < .01) greater than that in proximal segments. Total or subtotal occlusion occurred at the angioplasty site in 4 patients at the highest infused dose (10(-4) mol/L). The mean percent reduction in baseline diameter at previously dilated sites (53.8 +/- 5.9) at this dose was significantly (P < .05) greater than that observed at the adjacent proximal control sites and similar to that observed at distal control sites. All segments dilated significantly after intracoronary injection of isosorbide dinitrate. CONCLUSIONS. In dilated and nondilated vessels, serotonin caused significantly more marked constriction in distal than in proximal vessel segments. In dilated vessels, the vessel segments that had been subjected to angioplasty had a constrictor response to serotonin that was more marked than at adjacent proximal control sites and equivalent to that in the distal vessel segments. This enhanced constrictor response could be related to changes in endothelial cell function after regeneration or to hyperreactivity of smooth muscle cells at the angioplasty site.

This article has been cited by other articles:

				X. Lu, X. Guo, C. Linares, and G. S. Kassab A new method to denude the endothelium without damage to media: structural, functional, and biomechanical validation Am J Physiol Heart Circ Physiol, May 1, 2004; 286(5): H1889 - H1894. [Abstract] [Full Text] [PDF]

				E. D. Aymong, M. J. Curtis, M. Youssef, M. M. Graham, L. Shewchuk, W. Leschuk, and T. J. Anderson Abciximab Attenuates Coronary Microvascular Endothelial Dysfunction After Coronary Stenting Circulation, June 25, 2002; 105(25): 2981 - 2985. [Abstract] [Full Text] [PDF]

				C. Bauters, C. Amant, A. Boulier, P. Cabrol, E. McFadden, P. Duriez, M. E. Bertrand, and P. Amouyel Paraoxonase Polymorphism (Gln192Arg) as a Determinant of the Response of Human Coronary Arteries to Serotonin Circulation, February 22, 2000; 101(7): 740 - 743. [Abstract] [Full Text] [PDF]

				P. R. A. Caramori, V. C. Lima, P. H. Seidelin, G. E. Newton, J. D. Parker, and A. G. Adelman Long-term endothelial dysfunction after coronary artery stenting J. Am. Coll. Cardiol., November 15, 1999; 34(6): 1675 - 1679. [Abstract] [Full Text] [PDF]

				K. Miyata, H. Shimokawa, T. Yamawaki, I. Kunihiro, X. Zhou, T. Higo, E. Tanaka, N. Katsumata, K. Egashira, and A. Takeshita Endothelial Vasodilator Function Is Preserved at the Spastic/Inflammatory Coronary Lesions in Pigs Circulation, September 28, 1999; 100(13): 1432 - 1437. [Abstract] [Full Text] [PDF]

				E. Van Belle, C. Bauters, T. Asahara, and J. M. Isner Endothelial regrowth after arterial injury: from vascular repair to therapeutics Cardiovasc Res, April 1, 1998; 38(1): 54 - 68. [Full Text] [PDF]

				T. Sugiyama, K. Kawamura, H. Nanjo, M. Sageshima, and H. Masuda Loss of Arterial Dilation in the Reendothelialized Area of the Flow-Loaded Rat Common Carotid Artery Arterioscler Thromb Vasc Biol, November 1, 1997; 17(11): 3083 - 3091. [Abstract] [Full Text]

				T. Meurice, C. Bauters, J.-L. Auffray, B. Vallet, M. Hamon, F. Valero, E. Van Belle, J.-M. Lablanche, and M. E. Bertrand Basic Fibroblast Growth Factor Restores Endothelium-Dependent Responses After Balloon Injury of Rabbit Arteries Circulation, January 1, 1996; 93(1): 18 - 22. [Abstract] [Full Text]

				Y. Ozaki, D. Keane, and P. W. Serruys Progression and Regression of Coronary Stenosis in the Long-term Follow-up of Vasospastic Angina Circulation, November 1, 1995; 92(9): 2446 - 2456. [Abstract] [Full Text]