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

This Article Full Text (PDF) 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 Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wijns, W. Articles by Beckers, C. Search for Related Content PubMed PubMed Citation Articles by Wijns, W. Articles by Beckers, C.

Accumulation of Polymorphonuclears Leukocytes in Reperfused Ischemic Canine Myocardium: Relation with Tissue Viability Assessed by Fluorine- 18-2-Deoxy glucose Uptake

Center of Nuclear Medicine, the Positron Emission Tomography Laboratory, the Division of Cardiology and the Department of Pathology, University of Louvain, Brussels, Belgium

Correspondence: For reprints contact: William Wijns, MD, Positron Emission Tomography Laboratory, Avenue Hippocrate 55, Box 5550, B-1200 Brussels, Belgium.

ABSTRACT

Polymorphonudear leukocytes may participate in reperfusion injury. Whether leukocytes affect viable or only irreversibly injured tissue is not known. Therefore, we assessed the accumulation of ¹¹¹In-labeled leukocytes in tissue samples characterized as either ischemic but viable or necrotic by metabolic, histochemical, and ultrastructural criteria. Six open-chest dogs received left anterior descending coronary occlusion for 2 hr followed by 4 hr reperfusion. Myocardial blood flow was determined by microspheres and autologous ¹¹¹In labeled leukocytes were injected intravenously. Fluorine-18-2-deoxyglucose, a tracer of exogenous glucose utilization, was injected 3 hr after reperfusion. The dogs were killed 4 hr after reperfusion. The risk and the necrotic regions were assessed following in vivo dye injection and postmortem tetrazolium staining. Myocardial samples were obtained in the ischemic but viable, necrotic and normal zones, and counted for ¹¹¹In and ¹⁸F activity. Compared to normal,leukocytes were entrapped in necrotic regions(¹¹¹In activity: 207±73%) where glucose uptake was decreased(26 ± 15%). A persistent glucose uptake, marker of viability, was mainly seen in risk region(135 ± 85%) where leukocytes accumulation was moderate in comparison to normal zone (146 ± 44%). Thus, the glucose uptake observed in viable tissue is mainly related to myocytes metabolism and not to leukocytes metabolism

FOOTNOTES

Presented in part at the 34th Annual Meeting of the Society of Nuclear Medicine, Toronto, 1987.

This article has been cited by other articles:

				C. R. Bridges Myocardial laser revascularization: the controversy and the data Ann. Thorac. Surg., February 1, 2000; 69(2): 655 - 662. [Abstract] [Full Text] [PDF]

				K. Matsumura, R. W. Jeremy, J. Schaper, and L. C. Becker Progression of Myocardial Necrosis During Reperfusion of Ischemic Myocardium Circulation, March 3, 1998; 97(8): 795 - 804. [Abstract] [Full Text] [PDF]

				A. Maes, F. Van de Werf, J. Nuyts, G. Bormans, W. Desmet, and L. Mortelmans Impaired Myocardial Tissue Perfusion Early After Successful Thrombolysis : Impact on Myocardial Flow, Metabolism, and Function at Late Follow-up Circulation, October 15, 1995; 92(8): 2072 - 2078. [Abstract] [Full Text]