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This Article Full Text Full Text (PDF) All Versions of this Article: 288/6/H2763    most recent 00657.2004v1 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 Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Aouam, K. Articles by Ghaleh, B. Search for Related Content PubMed PubMed Citation Articles by Aouam, K. Articles by Ghaleh, B.

Preconditioning of salvaged myocardium in conscious rabbits with postinfarction dysfunction

¹Institut National de la Santé et de la Recherche Médicale (INSERM), Unité 660, Créteil; ²Ecole Nationale Vétérinaire d'Alfort, Maisons-Alfort; ³Fédération de Cardiologie de l'hôpital Henri Mondor, Créteil; and ⁴INSERM, Unité 652, Institut des Cordeliers, Paris, France; and ⁵Laboratoire de Pharmacologie, Faculté de Médecine de Monastir, Tunisia

Submitted 2 July 2004 ; accepted in final form 11 January 2005

Protection against postinfarction myocardial dysfunction is modest with classic preconditioning (PC). We investigated whether multiple cycles of PC could improve this protection and whether postinfarction dysfunction only depends on the amount of viable tissue. Eighteen rabbits were chronically instrumented with coronary occluders and ultrasonic crystals (segment shortening, SH) in the ischemic zone. A control group underwent 30-min coronary artery occlusion (CAO) with 72-h reperfusion (CAR). In two other groups, PC was induced by six 4-min CAO/4-min CAR cycles (PCx6) or one 5-min CAO/10-min CAR cycle (PCx1). After 72-h CAR, depression in SH was reduced in PCx1 (–68 ± 7% from baseline) and to a greater extent in PCx6 (–18 ± 10%) vs. control (–99 ± 7%; all P < 0.05). Infarct sizes were reduced in PCx1 (15 ± 2%) and to a greater extent in PCx6 (3 ± 1%) vs. control (46 ± 5%; P < 0.05). Contractility of salvaged myocardium was evaluated by calculating the ratio between SH at 72-h CAR and the amount of viable tissue. This index was enhanced in PCx1 (0.39 ± 0.07, P < 0.05) and to a greater extent in PCx6 (0.82 ± 0.09) vs. control (0.0 ± 0.10). This differential effect of PC was not related to changes in apoptosis, endothelial nitric oxide synthase (NOS) expression, or macrophages infiltration but, rather, to blunted inducible NOS expression in PCx6 vs. control and PCx1. Thus multiple cycles of PC induced an almost complete protection against postinfarction dysfunction, potentially involving beneficial effects on salvaged myocardium.

contractility; ischemia; cardioprotection; nitric oxide synthase

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