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J Thorac Cardiovasc Surg 1995;110:1606-1614
© 1995 Mosby, Inc.

CARDIOPULMONARY BYPASS,
MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

PRECONDITIONING WITH POTASSIUM CHANNEL OPENERS:A NEW CONCEPT FOR ENHANCING CARDIOPLEGIC PROTECTION?

Philippe Menasché, MD, PhD, Egidijus Kevelaitis, PhD (by invitation), Christian Mouas, (by invitation), Christian Grousset, MD, PhD (by invitation), Armand Piwnica, MD, Gérard Bloch, MD (by invitation)


Paris, France

From the Department of Cardiovascular Surgery and INSERM U-127, Hôspital Lariboisière, Paris, France.

Address for reprints: Philippe Menasché, MD, Department of Cardiovascular Surgery, Hôspital Lariboisière, 2 rue Ambroise Paré, 75475 Paris Cédex, France.

Abstract

Ischemic preconditioning defines an adaptive endogenous mechanism in which a brief episode of reversible ischemia renders the heart more resistant to a subsequent period of sustained ischemia. Because the cardioprotective effects of ischemic preconditioning might be mediated by an activation of adenosine triphosphate–sensitive potassium channels, this study was designed to assess whether these effects could be duplicated by the preischemic administration of a potassium channel opener. Fifty isolated isovolumic buffer-perfused rat hearts underwent 45 minutes of normothermic potassium arrest followed by 1 hour of reperfusion. They were divided into five equal groups that differed with regard to the preconditioning regimen: Group 1 hearts were left untreated and served as controls; in group 2, preconditioning was achieved with 5 minutes of total global ischemia followed by 5 minutes of buffer reperfusion before cardioplegic arrest; in group 3, the preconditioning stimulus consisted of a 5-minute infusion of the potassium channel opener nicorandil (10µmol/L) followed by 5 minutes of drug-free buffer perfusion before arrest; group 4 hearts underwent a similar protocol except that the infusion of nicorandil was preceded by that of the potassium channel blocker glibenclamide (10µmol/L); group 5 hearts were ischemically preconditioned like those of group 2 except that the no-flow preconditioning period was also preceded by a 5-minute infusion of glibenclamide (50µmol/L). The results demonstrate that ischemic preconditioning significantly improved contractility and reduced contracture during reperfusion, as compared with results in control hearts. These protective effects were duplicated by pretreatment with nicorandil but were abolished when the drug was antagonized by a prior infusion of glibenclamide. Likewise, the glibenclamide-induced blockade of potassium channels largely blunted the beneficial effects of ischemic preconditioning. These data suggest that opening of adenosine triphosphate–sensitive potassium channels substantially contributes to preconditioning-induced cardiac protection in a surgically relevant model of global ischemia and, consequently, that the use of potassium channel openers like nicorandil could be an effective means of enhancing cardioplegic protection. (J THORAC CARDIOVASC SURG 1995;110:1606-14)




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