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Ann Thorac Surg 1999;68:1920-1923
© 1999 The Society of Thoracic Surgeons


I. Pathophysiology of Ischemic Reperfusion Injury

Role of the ß2-integrins and immunoglobulin superfamily members in myocardial ischemia-reperfusion

Allan M. Lefer, PhDa

a Department of Physiology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania, USA

Address reprint requests to Dr Lefer, Department of Physiology, Jefferson Medical College, 1020 Locust St, Philadelphia, PA 19107;
e-mail: allan.m.lefer{at}mail.tju.edu

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

Abstract

Leukocytes play a key role in the inflammatory processes such as ischemia-reperfusion of the coronary vasculature. Their interaction with the endothelium is closely regulated. The first step in the process is the rolling of leukocytes (eg, neutrophils) along the microvascular endothelium. This is regulated by the selectin family of cell adhesion molecules, primarily P-selectin. The next step in the inflammatory cascade is the firm adhesion of these neutrophils to the activated or dysfunctional endothelium. This process is governed by the ß2-integrins on the leukocytes (eg, CD11/CD18) and by ICAM-1 on the activated endothelium. CD11/CD18 is a ß2-integrin, and ICAM-1 is a member of the immunoglobulin superfamily of adhesion glycoproteins. By their interaction, neutrophils flatten out and adhere to the vascular endothelium. Many of these adhered neutrophils are then able to transmigrate across the endothelium to the site of the inflammation (ie, the focus of the ischemia-reperfusion). This transmigration is primarily stimulated by PECAM-1, another member of the immunoglobulin superfamily. These processes are discussed in this brief review.




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