This Article Full Text 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 Qi, X.-L. Articles by Rouleau, J. L. Search for Related Content PubMed PubMed Citation Articles by Qi, X.-L. Articles by Rouleau, J. L. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB CAPTOPRIL Medline Plus Health Information Heart Attack Related Collections Cardiovascular Pharmacology Animal models of human disease Acute myocardial infarction Endothelium/vascular type/nitric oxide

(Circulation. 1999;100:1338-1345.)
© 1999 American Heart Association, Inc.

Basic Science Reports

Improvement of Endocardial and Vascular Endothelial Function on Myocardial Performance by Captopril Treatment in Postinfarct Rat Hearts

Xiu-Ling Qi, MD; Duncan J. Stewart, MD; Hugues Gosselin, DT; Azar Azad, PhD; Pierre Picard, PhD; Luc Andries, MD; Stanislas U. Sys, MD; Dirk L. Brutsaert, MD; Jean L. Rouleau, MD

From the Department of Medicine, Montreal Heart Institute, Montreal, Quebec (X.-L.Q., H.G., J.L.R.), and the Department of Medicine, St-Michael's Hospital, Toronto, Ontario (D.J.S., A.A., P.P.), Canada; and the Department of Physiology, University of Antwerp, Belgium (L.A., S.U.S., D.L.B.).

Correspondence to Dr Jean L. Rouleau, The Toronto Hospital, Division of Cardiology, 13EN-212–200 Elizabeth St, Toronto, Ontario M5G 2C4, Canada. E-mail jrouleau{at}torhosp.toronto.on.ca

Background—Endocardial (EE) and myocardial capillary vascular endothelial (myocap VE) cells have been shown to modulate the contractile characteristics of myocardium in a calcium-dependent manner. We evaluated the endothelial-myocardial interaction in the rat postinfarction myocardial infarction (MI) model and the effects of captopril.

Methods and Results—Wistar rats were divided into 4 groups treated for 4 weeks: (1) control; (2) infarcted controls (left anterior coronary artery ligation); (3) infarcted+captopril 2 g/L in drinking water; and (4) infarct+captopril+triton intracoronary injection. Coronary VE function was evaluated by infusion of serotonin in Langendorff preparations (n=31), and the myocardial contractile characteristics were investigated by use of isolated papillary muscles (n=44). Cardiac mRNA for endothelial constitutive nitric oxide synthase (ecNOS) was measured, and its cellular location was evaluated by immunohistochemistry. Serotonin-induced increase in coronary flow was decreased in infarct controls compared with controls (4.6% versus 53.4%, P<0.01) but not in the 2 infarct+captopril groups. Intracoronary triton injection decreased serotonin-induced coronary flow in the infarct+captopril+triton group. All MI groups had decreased total tension in isolated papillary muscles. EE removal by triton immersion decreased total tension in all groups except for infarct controls (3.3 versus 3.2 g/mm²). Cardiac ecNOS mRNA decreased in the control infarct group but remained normal in the infarct+captopril group.

Conclusions—Chronic postinfarction endothelium-induced coronary vasodilatation is impaired, and both EE and myocap VE dysfunction contribute to myocardial depression. Captopril use prevents these abnormalities and the reduction of cardiac ecNOS mRNA.

Key Words: myocardial infarction • endothelium • contractility • heart failure

This article has been cited by other articles:

				N. S. Dhalla, M. R. Dent, P. S. Tappia, R. Sethi, J. Barta, and R. K. Goyal Subcellular Remodeling as a Viable Target for the Treatment of Congestive Heart Failure Journal of Cardiovascular Pharmacology and Therapeutics, March 1, 2006; 11(1): 31 - 45. [Abstract] [PDF]

				U. Landmesser, N. Engberding, F. H. Bahlmann, A. Schaefer, A. Wiencke, A. Heineke, S. Spiekermann, D. Hilfiker-Kleiner, C. Templin, D. Kotlarz, et al. Statin-Induced Improvement of Endothelial Progenitor Cell Mobilization, Myocardial Neovascularization, Left Ventricular Function, and Survival After Experimental Myocardial Infarction Requires Endothelial Nitric Oxide Synthase Circulation, October 5, 2004; 110(14): 1933 - 1939. [Abstract] [Full Text] [PDF]

				D. L. Brutsaert Cardiac Endothelial-Myocardial Signaling: Its Role in Cardiac Growth, Contractile Performance, and Rhythmicity Physiol Rev, January 1, 2003; 83(1): 59 - 115. [Abstract] [Full Text] [PDF]

				J. Bauersachs, M. Heck, D. Fraccarollo, S. K. Hildemann, G. Ertl, M. Wehling, and M. Christ Addition of spironolactone to angiotensin-converting enzyme inhibition in heart failure improves endothelial vasomotor dysfunction: Role of vascular superoxide anion formation and endothelial nitric oxide synthase expression J. Am. Coll. Cardiol., January 16, 2002; 39(2): 351 - 358. [Abstract] [Full Text] [PDF]

				J. Bauersachs, P. Galuppo, D. Fraccarollo, M. Christ, and G. Ertl Improvement of Left Ventricular Remodeling and Function by Hydroxymethylglutaryl Coenzyme A Reductase Inhibition With Cerivastatin in Rats With Heart Failure After Myocardial Infarction Circulation, August 28, 2001; 104(9): 982 - 985. [Abstract] [Full Text] [PDF]

				A. I. M. Al-Shafei, R. G. Wise, G. A. Gresham, G. Bronns, T. A. Carpenter, L. D. Hall, and C. L.-H. Huang Non-invasive magnetic resonance imaging assessment of myocardial changes and the effects of angiotensin-converting enzyme inhibition in diabetic rats J. Physiol., January 9, 2002; 538(2): 541 - 553. [Abstract] [Full Text] [PDF]

				A. I. M. Al-Shafei, R. G. Wise, G. A. Gresham, T. A. Carpenter, L. D. Hall, and C. L.-H. Huang Magnetic resonance imaging analysis of cardiac cycle events in diabetic rats: the effect of angiotensin-converting enzyme inhibition J. Physiol., January 9, 2002; 538(2): 555 - 572. [Abstract] [Full Text] [PDF]