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J Thorac Cardiovasc Surg 2000;119:842-848
© 2000 The American Association for Thoracic Surgery

CARDIOPULMONARY SUPPORT AND PHYSIOLOGY

ADENOSINE TRIPHOSPHATE–DEPENDENT POTASSIUM CHANNEL MODULATION AND CARDIOPLEGIA-INDUCED PROTECTION OF HUMAN ATRIAL MUSCLE IN AN IN VITRO MODEL OF MYOCARDIAL STUNNING

From the Laboratory of Cardiovascular Pharmacology, Department of Cardiac Surgery and Second Section of Cardiology, University of Rome "La Sapienza," Rome, Italy.

Supported in part by Ministero dell’Università e della Ricerca Scientifica, Rome (Ricerche di Ateneo 145/1997) and by Cardioricerca, Rome, Italy. Dr Wagner from E. Merck, Darmstadt, Germany, provided a gift of bimakalim used in this study.

Address for reprints: Paolo Emilio Puddu, MD, FESC, FACC, Istituto di Chirurgia del Cuore e Grossi Vasi, II Cattedra di Cardiologia, Università degli Studi di Roma "La Sapienza," Viale del Policlinico, 155, Rome 00161, Italy (E-mail: puddu.pe{at}iol.it ).

Objectives: Although adenosine triphosphate–dependent potassium channel openers have been shown to enhance cardioplegic protection in animal myocardium, there is a lack of data on human cardiac tissues. We aimed at determining, on human atrial muscle, whether adenosine triphosphate– dependent potassium channels are involved in protection caused by high-potassium cardioplegia and whether adenosine triphosphate–dependent potassium channel activation might improve cardioplegic protection in an in vitro model of myocardial stunning.
Methods: Human atrial trabeculae were obtained from adult patients undergoing cardiac operations. In an organ bath at 37°C, the preparations were subjected to 60 minutes of hypoxia at a high stimulation rate either in Tyrode solution (control, n = 17) or in St Thomas’ Hospital solution without additives (n = 6) or associated with 100 nmol/L bimakalim (n = 7) or 1 µmol/L glibenclamide (n = 7), followed by 60 minutes of reoxygenation and 15 minutes of positive inotropic stimulation with 1 µmol/L dobutamine.
Results: Atrial developed tension was reduced by hypoxia to 27% ± 5% of baseline and incompletely recovered after reoxygenation to 38% ± 7%, whereas dobutamine restored contractility to 74% ± 7% of basal values. St Thomas’ Hospital solution with or without bimakalim improved developed tension after reoxygenation and dobutamine (P < .0001 vs control), whereas glibenclamide inhibited these protective effects of cardioplegic arrest (P = .001 vs St Thomas’ Hospital solution). After reoxygenation, the protective effect of bimakalim disappeared at a high pacing rate (400- and 300-ms cycle length) but recovered during dobutamine superfusion.
Conclusions: Adenosine triphosphate–dependent potassium channels are likely involved in the cardioprotective effects of cardioplegia in human atrial trabeculae and adenosine triphosphate–dependent potassium channel activation with bimakalim used as an additive to cardioplegia enhanced protection.

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