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Eur J Cardiothorac Surg 2005;27:111-116
© 2005 Elsevier Science NL

Na⁺/H⁺ exchange inhibition in hypertrophied myocardium subjected to cardioplegic arrest: an effective cardioprotective approach

^a Department of Cardiovascular Surgery, Hôpital Europeen Georges Pompidou and INSERM u-633, 20-40, rue Leblanc, 75908 Paris cedex 15, France
^b INSERM U-572, Hôpital Lariboisière, Paris, France
^c Department of Physiology and Heart Centre, Kaunas University of Medicine, Kaunas, Lithuania
^d Centre for Cardiovascular Biology and Medicine, The Rayne Institute, St Thomas' Hospital, London, UK

Received 19 April 2004; received in revised form 12 August 2004; accepted 23 August 2004.

^* Corresponding author. Tel.: +33 1 56 09 29 62; fax: +33 1 56 09 22 19. (E-mail: philippe.menasche{at}hop.egp.ap-hop-paris.fr).

Objective: This study was designed to assess whether the protective effects of Na⁺/H⁺ exchange (NHE) inhibition, which have been largely demonstrated in normal hearts, are also manifest in a more surgically relevant model of hypertrophied myocardium subjected to cardioplegic arrest. Methods: Left ventricular hypertrophy was created in 3-week-old rats by coarctation of the ascending thoracic aorta with a hemoclip. Eight weeks later, hearts were excised, isovolumetrically perfused and subjected to 1h of potassium cardioplegic arrest followed by 2h of reperfusion. Hearts were allocated to one of the following four groups: sham-operated and aortic banding hearts without any treatment or treated with the NHE inhibitor cariporide (1µmol/L) given as an additive to cardioplegia and over the first 15min of reperfusion. Results: The major effect of cariporide was to reduce ischemic peak contacture and to improve post-ischemic diastolic function in both sham-operated and hypertrophied hearts. Total creatine kinase release over the first 45min of reperfusion was significantly reduced in hypertrophied hearts treated with cariporide. The endothelium-dependent coronary vasodilation to 5-hydroxytryptamine was observed in all sham-operated hearts before cardiac arrest, however, it was significantly impaired following cardioplegic ischemia and reperfusion. Hypertrophied hearts demonstrated markedly impaired endothelium-dependent and -independent coronary vasodilations during both pre- and post-ischemic period that were not affected by the treatment with cariporide. Conclusions: The cardioprotective effects of the NHE inhibitor cariporide are also manifest in hypertrophied myocardium, which supports the potential usefulness of NHE inhibition in the setting of cardiac surgery.

Key Words: Cardioplegia • Ischemia/reperfusion • Left ventricular function • Myocardial injury • Myocardial hypertrophy • Na+/H+exchange inhibitor