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American Journal of Pathology, Vol 143, 464-472, Copyright © 1993 by American Society for Investigative Pathology

REGULAR ARTICLES

Role of beta 2 integrins and ICAM-1 in lung injury following ischemia- reperfusion of rat hind limbs

A Seekamp, MS Mulligan, GO Till, CW Smith, M Miyasaka, T Tamatani, RF Todd 3d and PA Ward
Department of Pathology, University of Michigan Medical School, Ann Arbor 48109-0602.

Ischemia/reperfusion involving the hind limbs of rats results in both local injury to skeletal muscle as well as injury to lungs, as measured by increased vascular permeability (125I-labeled bovine serum albumin leakage) and hemorrhage (extravasation of 51Cr-labeled rat erythrocytes). In the current study, we have focused on events in lungs occurring during reperfusion of hind limbs. Analysis of blood neutrophils obtained 4 hours after reperfusion has indicated up- regulation of CD11b and CD18 but not CD11a. Plasma from the same animals demonstrate the ability to induce similar effects in normal blood neutrophils, indicative of the presence of a neutrophil- activating agent in plasma. During reperfusion, lung injury, which develops progressively over a 4-hour period, has been shown to be neutrophil-dependent and requires CD11a/CD18 and CD11b/CD18 as well as intercellular adhesion molecule-1. These data suggest that ischemia and reperfusion injury of rat lower extremities causes systemic changes that result in neutrophil-dependent lung injury that is beta 2 integrin- (leukocyte function antigen-1, Mac-1) and intercellular adhesion molecule-1-dependent.

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