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Articles in PresS, published online ahead of print November 29, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00909.2001
Submitted on October 18, 2001
Accepted on November 26, 2001
1 Department of Medicine, University of California San Diego, San Diego, CA, USA; Department of Medicine, University of Naples Federico II, Napoli, Italy, Italy
2 Department of Experimental Pharmacology, University of Naples Fedeico II, Napoli, Italy, Italy
3 Department of Pharmacology & Therapeutics, University of Calgary, Calgary, Alberta, Canada
4 Department of Medicinal Chemistry, University of Naples Fedrico II, Napoli, Italy, Italy
5 Department of Medicine, University of Naples Federico II, Napoli, Italy, Italy
* To whom correspondence should be addressed. E-mail: cirino{at}unina.it.
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 (LV Developed pressure, LV 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, following 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.
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