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The FASEB Journal, Vol 5, 2529-2537, Copyright © 1991 by The Federation of American Societies for Experimental Biology
REVIEWS |
ML Entman, L Michael, RD Rossen, WJ Dreyer, DC Anderson, AA Taylor and CW Smith
Section of Cardiovascular Sciences, Methodist Hospital, Houston, Texas.
Experimental models of acute ischemic myocardial injury indicate that the inflammatory response after the ischemic event contributes to tissue damage. This is especially apparent with reperfusion of the ischemic tissue. In such models some therapeutic strategies designed to reduce neutrophil accumulation or function have resulted in apparently beneficial effects. Although such findings are encouraging, interventions into these pathological processes using specific molecular targets will require greater understanding of specific mechanisms. Current evidence indicates that potential sites of therapeutic intervention will be found in pathways leading to complement activation, generation of lipid-derived mediators, adhesion of neutrophils to endothelial cells and cardiac myocytes, and activation of neutrophil secretory processes releasing, for example, proteolytic enzymes and reactive oxygen. Understanding the dynamic interplay between the mediators, adhesion pathways, and secretory processes that results in myocardial damage will allow a rational approach to controlling the detrimental inflammatory consequences of ischemia and reperfusion.
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F.-J. Neumann, I. Ott, M. Gawaz, G. Richardt, H. Holzapfel, M. Jochum, and A. Schomig Cardiac Release of Cytokines and Inflammatory Responses in Acute Myocardial Infarction Circulation, August 15, 1995; 92(4): 748 - 755. [Abstract] [Full Text]
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P. R. Hansen Role of Neutrophils in Myocardial Ischemia and Reperfusion Circulation, March 15, 1995; 91(6): 1872 - 1885. [Abstract] [Full Text]
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J. P. Mathew, C. S. Rinder, J. B. Tracey, L. A. Auszura, T. O'Connor, E. Davis, and B. R. Smith Acadesine inhibits neutrophil CD11b up-regulation in vitro and during in vivo cardiopulmonary bypass J. Thorac. Cardiovasc. Surg., March 1, 1995; 109(3): 448 - 456. [Abstract] [Full Text]
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M. Buerke, T. Murohara, and A. M. Lefer Cardioprotective Effects of a C1 Esterase Inhibitor in Myocardial Ischemia and Reperfusion Circulation, January 15, 1995; 91(2): 393 - 402. [Abstract] [Full Text]
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Y. Sawa, H. Matsuda, Y. Shimazaki, M. Kaneko, M. Nishimura, A. Amemiya, K. Sakai, and S. Nakano Evaluation of leukocyte-depleted terminal blood cardioplegic solution in patients undergoing elective and emergency coronary artery bypass grafting J. Thorac. Cardiovasc. Surg., December 1, 1994; 108(6): 1125 - 1131. [Abstract] [Full Text]
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H. A. Hennein, H. Ebba, J. L. Rodriguez, S. H. Merrick, F. M. Keith, M. H. Bronstein, J. M. Leung, D. T. Mangano, L. J. Greenfield, and J. S. Rankin Relationship of the proinflammatory cytokines to myocardial ischemia and dysfunction after uncomplicated coronary revascularization J. Thorac. Cardiovasc. Surg., October 1, 1994; 108(4): 626 - 635. [Abstract] [Full Text]
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L. G. Lange and G. F. Schreiner Immune Mechanisms of Cardiac Disease N. Engl. J. Med., April 21, 1994; 330(16): 1129 - 1135. [Full Text]
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C. Napoli, F. De Nigris, C. Cicala, J. L. Wallace, G. Caliendo, M. Condorelli, V. Santagada, and G. Cirino Protease-activated receptor-2 activation improves efficiency of experimental ischemic preconditioning Am J Physiol Heart Circ Physiol, June 1, 2002; 282(6): H2004 - H2010. [Abstract] [Full Text] [PDF]
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