HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Nguyen, D. Articles by Shennib, H. Search for Related Content PubMed PubMed Citation Articles by Nguyen, D. Articles by Shennib, H.

The Journal of Thoracic and Cardiovascular Surgery, Vol 101, 1030-1036, Copyright © 1991 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association

ARTICLES

Warm ischemia induces alteration in lung immune cell functions

D Nguyen, DS Mulder and H Shennib
McGill University Lung Transplant Program, Montreal, Quebec, Canada.

Warm ischemia is an important factor in early allograft dysfunction. To elucidate cellular events involved in such lung injury, we examined the effects of warm ischemia on the cytotoxic function of lymphocytes retrieved by bronchoalveolar lavage as compared with peripheral blood lymphocytes. Warm ischemia of the lung was induced in eight dogs by crossclamping left hilar structures for 1 hour. Bronchoalveolar cells from ischemia left and unaffected right lungs, as well as blood lymphocytes, were isolated before operation and 2 hours, 72 hours, and 7 days after operation. Lung and blood lymphocytes were assayed for natural killer and lectin-dependent cell-mediated cytotoxicity. Warm ischemia resulted in a significant impairment of natural killer activity within 2 hours of reperfusion (49% of preoperative control cytolysis, p less than 0.01). There was a significant increase in natural killer activity in bronchoalveolar lavage mononuclear cells 72 hours after reperfusion injury (178.4% of preoperative value, p less than 0.01). Interestingly, these functional alterations were not paralleled with changes seen in the peripheral blood lymphocytes or the opposite nonaffected lungs, where the natural killer activity appeared significantly depressed at 72 hours. Similarly, lectin-dependent cell- mediated cytotoxicity was noted to be increased in the bronchoalveolar lavage from the ischemic lung (179.5%, p less than 0.01) but decreased in the bronchoalveolar lavage from the nonaffected lung and peripheral blood lymphocytes at 72 hours after injury. We conclude that warm ischemia is associated with a functional alteration of the local lung immune cells. Such alteration is not observed in cells from the opposite lung or peripheral blood. The observed increase in nonspecific cytotoxicity of bronchoalveolar lymphocytes can be causative in the early damage seen in poorly preserved lung allografts.

This article has been cited by other articles:

				C. Serrick, A. Giaid, A. Reis, and H. Shennib Prolonged Ischemia Is Associated With More Pronounced Rejection in the Lung Allograft Ann. Thorac. Surg., January 1, 1997; 63(1): 202 - 208. [Abstract] [Full Text]

				T. Shiraishi, T. Mizuta, S. R. DeMeester, J. H. Ritter, P. E. Swanson, M. R. Wick, J. D. Cooper, and G. A. Patterson Effect of Ischemic Injury on Subsequent Rat Lung Allograft Rejection Ann. Thorac. Surg., October 1, 1995; 60(4): 947 - 951. [Abstract] [Full Text]