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Ann Thorac Surg 1999;68:1949-1953
© 1999 The Society of Thoracic Surgeons

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I. Pathophysiology of Ischemic Reperfusion Injury

Treating myocardial ischemia-reperfusion injury by targeting endothelial cell transcription

^a Divisions of Cardiothoracic Surgery, and Trauma and Critical Care, Department of Surgery, University of Washington, Seattle, Washington, USA

Address reprint requests to Dr Verrier, Division of Cardiothoracic Surgery, University of Washington, Box 356310, 1959 NE Pacific, Seattle, WA 98195-6310
e-mail: edver{at}u.washington.edu

Presented at the International Symposium on Myocardial Protection From Surgical Ischemic-Reperfusion Injury, Asheville, NC, Sept 21–24, 1997.

Abstract

Exacerbation of, rather than improvement in, a hypoxic injury after reperfusion of ischemic tissues is recognized as the specific clinicopathologic entity referred to as ischemia/reperfusion (I/R) injury. Arguably, one of the most common forms of I/R injury occurs during cardiac surgery, which has a mandatory period of myocardial ischemia required to allow surgery in a bloodless, motionless field, followed by coronary artery reperfusion after removal of the aortic cross-clamp. In this review, we examine the endothelial cell activation phenotype that initiates and propagates myocardial I/R injury. Emphasis is given to the biology of one transcription factor, NF-B, that has the principal role in the regulation of many endothelial cell genes expressed in activated endothelium. NF-B-dependent transcription of endothelial cell genes that are transcribed in response to I/R injury may be a favorable approach to preventing tissue injury in the setting of I/R. Elucidating safe and effective therapy to inhibit transcription of endothelial cell genes involved in promoting injury after I/R injury may have wide applicability to the patients with heart disease and other forms of I/R injury.

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