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Am J Physiol Heart Circ Physiol 282: H2004-H2010, 2002. First published November 29, 2001; doi:10.1152/ajpheart.00909.2001
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Vol. 282, Issue 6, H2004-H2010, June 2002

Protease-activated receptor-2 activation improves efficiency of experimental ischemic preconditioning

Claudio Napoli1,5, Filomena De Nigris1,5, Carla Cicala2, John L. Wallace6, Giuseppe Caliendo4, Mario Condorelli1, Vincenzo Santagada4, and Giuseppe Cirino2

Departments of 1 Medicine, 2 Experimental Pharmacology, and 3 Medicinal Chemistry, Federico II University of Naples; 4 Department of Medicinal Chemistry, Domenico Montesano 49, 80131 Naples, Italy; 5 Department of Medicine, University of California, San Diego, California 92093; and 6 Department of Pharmacology and Therapeutics, University of Calgary, Alberta, Canada

Protease-activated receptor-2 (PAR-2) is a member of seven transmembrane domain G protein-coupled receptors activated by proteolytic cleavage. PAR-2 is involved in inflammatory events and cardiac ischemic reperfusion injury. The objective of this study was to investigate the effects of PAR-2 in experimental myocardial ischemic preconditioning. To monitor the effects of PAR-2, Langendorff-perfused rat hearts were used. These hearts were treated with PAR-2-activating peptide (PAR-2AP) in various protocols. Hemodynamic parameters (left ventricular developed pressure, left ventricular diastolic pressure, coronary flow rate, and heart rate), several indexes of oxidative injury, and neutrophil accumulation were evaluated. We show for the first time that enhanced PAR-2 activation improves efficiency of ischemic preconditioning and reduces cardiac inflammation in the rat heart. Indeed, after PAR-2AP infusion we found that hemodynamic parameters, oxidative injury, infarct size, and neutrophil accumulation were involved. These data support the concept that PAR-2-dependent cell trafficking may regulate signaling responses to cardiac ischemia and inflammation.

heart; inflammation


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