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J Thorac Cardiovasc Surg 1997;113:932-941
© 1997 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

DEPOLARIZING CARDIAC ARREST AND ENDOTHELIUM-DERIVED HYPERPOLARIZING FACTOR–MEDIATED HYPERPOLARIZATION AND RELAXATION IN CORONARY ARTERIES: THE EFFECT AND MECHANISM

Supported by a Committee of Research and Conference Grant (337/048/0018) and a Vice-Chancellor Grant (SN/mp/350/172/0/9), University of Hong Kong.

Received for publication March 21, 1996 revisions requested May 23, 1996; revisions received August 12, 1996 accepted for publication August 12, 1996. Address for reprints: Professor Guo-Wei He, MD, PhD, Chair of Cardiothoracic Surgery, University of Hong Kong, The Grantham Hospital, 125 Wong Chuk Hang Rd., Aberdeen, Hong Kong.

Abstract

Objectives: Depolarizing (hyperkalemic) solutions are widely used to preserve organs for transplantation and for cardiac operations. We previously observed that exposure to hyperkalemia reduced endothelium-dependent, noncyclooxygenase- and non–nitric oxide–mediated relaxation. This study was designed to examine the mechanism of this effect with regard to K channels and the associated membrane potential changes.Methods: Porcine coronary artery rings were studied in organ chambers. After incubation of the tissue with 20 or 50 mmol/L doses of potassium for 1 hour, the endothelium-derived hyperpolarizing factor–mediated relaxation in the artery and the membrane hyperpolarization in a single coronary smooth muscle cell were studied.Results: The endothelium-derived hyperpolarizing factor–mediated relaxation induced by substance P, which could be significantly inhibited by the Ca²⁺-activated K channel blocker tetraethylammonium but only to a lesser extent by the adenosine triphosphate–sensitive K channel blocker glibenclamide, was significantly reduced. Substance P–induced hyperpolarization of the membrane potential was also significantly reduced by the hyperkalemic incubation with a significantly elevated resting membrane potential.Conclusions: Depolarizing arrest reduces endothelium-derived hyperpolarizing factor–mediated membrane hyperpolarization and relaxation by affecting mainly the Ca²⁺-activated K channels and by depolarizing the membrane for a prolonged period. We suggest that this is one of the mechanisms for coronary dysfunction after exposure to depolarizing (hyperkalemic) cardioplegic and organ-preservation solutions and that, therefore, "perfect" protection of the heart or other organs should restore the endothelium-derived hyperpolarizing factor–related endothelial function.

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