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      PMN/Platelets Coinfused in Guinea Pig Hearts Exposed to Low-Flow Ischemia Have no Additive Cardiodepressive Effect

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          Recent studies revealed an additive cardiodepressive effect of polymorphonuclear granulocytes (PMN) and thrombocytes in hearts exposed to a no-flow ischemia. To find out whether or not this is also true for isolated guinea pig hearts exposed to a low-flow ischemia, the current study was performed. PMN or thrombocytes, together or separately, were applied as a 1-min bolus (1,000/µl or 20,000/µl, respectively) during ischemia or in reperfusion in the presence of thrombin (0.3 U/ml perfusate). Recovery of external heart work and intracoronary cell retention were quantified in percent. Sole application of PMN or platelets during ischemia and reperfusion significantly compromised myocardial function, whereas coapplication of PMN and platelets did not exhibit any further cardiodepressive effect. Coapplication of cells almost prevented intracoronary platelet retention during ischemia and in reperfusion, as opposed to sole platelet application. Known blockers of endogenously released anti-platelet substances like nitric oxide, PGI<sub>2</sub> or adenosine did not mediate a further aggravation of myocardial dysfunction. The platelet-activating factor (PAF) antagonist WEB 2170 BS, however, significantly improved recovery of external heart work during ischemia and in reperfusion. This indicates that an additive cardiodepressive effect of PMN and platelets in working guinea pig hearts exposed to a low-flow ischemia, cannot be demonstrated, whereas PAF antagonists seem to be cardioprotective, under these conditions. Even addition of fibrinogen to the perfusate, did not show an additive cardiodepressive effect of coapplication of PMN and platelets.

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          Most cited references 5

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          Molecular mechanisms of leukocyte recruitment in the inflammatory process.

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          The microcirculation constitutes the functional interface between the circulating blood and the interstitial space. To gain access to sites of inflammation, leukocytes must pass the endothelial barrier. The recruitment paradigm encompasses leukocyte margination, capture, rolling, activation, firm adhesion, and transmigration. Recent experimental work has shown that E-, L- and P-selectins and alpha 4 integrins can mediate leukocyte rolling. Upon activation by chemokines, complement peptides or lipid mediators, firm adhesion is afforded by beta 1 and beta 2 integrins, InterCellular Adhesion Molecules (ICAMs) and Vascular Cell Adhesion Molecule-1 (VCAM-1). Beta 1 and beta 2 integrins as well as Platelet-Endothelial Cell Adhesion Molecule-1 (PECAM-1) have been shown to be involved in transmigration. Intravital microscopic techniques have been instrumental in applying the conceptual advances of cell and molecular biology to the in vivo situation. This review focuses on the current understanding of the leukocyte recruitment paradigm as suggested by in vivo observations and in vitro model systems. The paradigm of neutrophil recruitment is presented to serve as a model for the recruitment mechanisms of other inflammatory cells.
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            Chemokines and the Arrest of Lymphocytes Rolling Under Flow Conditions

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              Adenosine endogenously released during early reperfusion mitigates postischemic myocardial dysfunction by inhibiting platelet adhesion


                Author and article information

                J Vasc Res
                Journal of Vascular Research
                S. Karger AG
                December 2003
                29 January 2004
                : 40
                : 6
                : 501-508
                aMedizinische Klinik II mit Poliklinik, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, and bDepartment of Cardiology, University Hospital Benjamin Franklin, Free University of Berlin, Berlin, Germany
                74890 J Vasc Res 2003;40:501–508
                © 2003 S. Karger AG, Basel

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                Page count
                Figures: 7, References: 24, Pages: 8
                Research Paper


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