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1 Dipartimento di Scienze Cliniche e Biologiche, Universita degli Studi di Torino, Orbassano, TO, Italy
2 Dipartimento di Biologia Animale e del Uomo, Universita degli Studi di Torino, Torino, TO, Italy
* To whom correspondence should be addressed. E-mail: giuseppe.alloatti{at}unito.it.
Ischemic preconditioning (IP) is a cardioprotective mechanism against myocellular death and cardiac dysfunction resulting from reperfusion of ischemic heart. At present, the precise list of mediators involved in IP and the pathways of their mechanisms of action are not completely known. The aim of the present study was to investigate the role of platelet activating factor (PAF), a phospholipid mediator which is known to be released by ischemic-reperfused heart, as a possible endogenous agent involved in IP. Experiments were performed on Langendorff-perfused rat hearts undergoing 30 minutes of ischemia followed by 2 hours of reperfusion. Treatment with a low concentration of PAF (2x10-11 M) before ischemia reduced the extension of infarct size and improved the recovery of left ventricular developed pressure during reperfusion. The cardioprotective effect of PAF was comparable to that observed in hearts in which IP was induced by three brief (3 min) periods of ischemia separated by 5 min reperfusion intervals. The PAF receptor antagonist WEB 2170 (1x10-9 M) abrogated the cardioprotective effect induced by both PAF and IP. The protein kinase C (PKC) inhibitor chelerythrine (5x10-6 M) or the phosphoinositide 3-kinase (PI3K) inhibitor LY 294002 (5x10-5 M) also reduced the cardioprotective effect of PAF. Western blot analysis revealed that following IP treatment or PAF infusion, the phosphorylation of PKC-epsilon and Akt (the downstream target of PI3K) was higher than in control hearts. The present data indicate that exogenous applications of low quantities of PAF induce a cardioprotective effect, through PI3K and PKC activation, similar to that afforded by IP. Moreover, the study suggests that endogenous release of PAF, induced by brief periods of ischemia and reperfusion, may participate to the triggering of the IP of the heart.
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