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Am J Physiol Heart Circ Physiol 276: H1574-H1580, 1999;
0363-6135/99 $5.00
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Vol. 276, Issue 5, H1574-H1580, May 1999

L-Arginine limits myocardial cell death secondary to hypoxia-reoxygenation by a cGMP-dependent mechanism

Luis Agulló, David García-Dorado, Javier Inserte, Amaya Paniagua, Pasi Pyrhonen, Joan Llevadot, and Jordi Soler-Soler

Servicio de Cardiología, Hospital General Universitario Vall d'Hebron, 08035 Barcelona, Spain

The objective of this study was to investigate the effect of L-arginine supplementation on myocardial cell death secondary to hypoxia-reoxygenation. Isolated rat hearts (n = 51) subjected to 40 min of hypoxia and 90 min of reoxygenation received 3 mM L-arginine and/or 1 µM 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; a selective inhibitor of soluble guanylyl cyclase) throughout the experiment or during the equilibration, hypoxia, or reoxygenation periods. The incorporation of L-[3H]arginine into myocytes during energy deprivation was investigated in isolated adult rat myocytes. The addition of L-arginine to the perfusate throughout the experiment resulted in higher cGMP release (P < 0.05), reduced lactate dehydrogenase release (P < 0.05), and increased pressure-rate product (P < 0.05) during reoxygenation. These effects were reproduced when L-arginine was added only during equilibration, but addition of L-arginine during hypoxia or reoxygenation had no effect. Addition of ODQ either throughout the experiment or only during reoxygenation reversed the beneficial effects of L-arginine. L-[3H]arginine was not significantly incorporated into isolated myocytes subjected to energy deprivation. We conclude that L-arginine supplementation protects the myocardium against reoxygenation injury by cGMP-mediated actions. To be effective during reoxygenation, L-arginine must be added before anoxia.

isolated rat heart; reperfusion; contractile function; nitric oxide; guanylyl cyclase inhibition; myocytes; uptake


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