Acta Physiologica 2010; Volume 200, Supplement 681
Abstracts of the 61st National Congress of the Italian Physiological Society
GROWTH HORMONE-RELEASING HORMONE (GHRH) INDUCES CARDIOPROTECTION IN ISOLATED RAT HEART AKIN TO ISCHEMIC POSTCONDITIONING
Abstract number: P2
ALLOATTI1,4 G, TULLIO2,4 F, SETTANNI3 F, GHIGO3 E, GRANATA3 R, PENNA2,4 C
1Dip. Biologia Animale e dellUomo, Univ. Torino, Italy
2Dip. Scienze Cliniche e Biologiche, Univ. Torino, Italy
3Dip. Medicina Interna, Univ. Torino, Italy
4Istituto Nazionale per la Ricerca Cardiovascolare, Bologna, Italy
It has been recently shown that infusion of hypothalamic neuropeptide GHRH before ischemia significantly reduced ischemia/reperfusion (I/R) injury. The cardioprotective effect of GHRH was due to activation of Reperfusion Ischemic Survival Kinases (RISK) pathway. Since, however, a treatment carried out after the ischemic insult (e.g. Postconditioning; PostC) is a more feasible practice for clinical application, we also studied the action of GHRH given during reperfusion on the activation of RISK pathway, the infarct size (IS) and the cardiac performance.
Isolated rat hearts perfused at constant flow were subjected to: a) 30 min ischemia (I) and 120 min R (I/R), b) PostC (5 cycles of 10 s I/R at the beginning of R), c) GHRH-R (50 nM) during the first 20 min of R. We assessed left ventricular end-diastolic and developed pressures (LVDP) during R, IS and kinases phosphorylation (western blotting) at the end of R.
IS (61±4% of risk area in I/R) was significantly reduced in PostC and GHRH-R Groups (28±3 and 17±2%). At the end of reperfusion, GHRH-R showed preserved cardiac performance, comparable to pre-I levels. Western blotting analysis demonstrated the activation of other kinases (STAT-3 and AMPK) besides those included in RISK pathway, such as Akt/PKB and Gsk3b.
Our results demonstrate that, like PostC, GHRH given during early reperfusion exerts cardioprotective effects, enhancing LVDP and reducing IS and development of diastolic contracture.
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Acta Physiologica 2010; Volume 200, Supplement 681 :P2