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Ann Thorac Surg 2003;75:S667-S673
© 2003 The Society of Thoracic Surgeons

I: Pathophysiology of ischemic-reperfusion injury

The mitochondrial KATP channel and cardioprotection

James D. McCully, PhDa*, Sidney Levitsky, MDa

a Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA

* Address reprint requests to Dr McCully, Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, 77 Avenue Louis Pasteur, Room 144, Boston, MA 02115, USA
e-mail: jamesmccully{at}hms.harvard.edu

Presented at the 3rd International Symposium on Myocardial Protection From Surgical Ischemic-Reperfusion Injury, Asheville, NC, June 2–6, 2002.

Abstract

Adenosine triphosphate (ATP)–sensitive potassium (KATP) channels allow coupling of membrane potential to cellular metabolic status. Two KATP channel subtypes coexist in the myocardium, with one subtype located in the sarcolemma (sarcKATP) membrane and the other in the inner membrane of the mitochondria (mitoKATP). The KATP channels can be pharmacologically modulated by a family of structurally diverse agents of varied potency and selectivity, collectively known as potassium channel openers and blockers. Sufficient evidence exists to indicate that the KATP channels and, in particular, the mitoKATP channels play an important role both as a trigger and an effector in surgical cardioprotection. In this review, the biochemistry and surgical specificity of the KAtp channels are examined.




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