One of the possible mechanisms of this antiarrhythmic protection is that nitric oxide may inactivate superoxide radicals during reperfusion . Similarly, inhibition of nitric oxide synthase with L-NAME augmented ischemia-reperfusion injury in rabbit hearts in vivo . Thus, nitric oxide appears to function as an endogenous cardioprotectant not only in the canine but also in rats and rabbits. Maulik and colleagues demonstrated that nitric oxide plays an important role in transmembrane signalling in the ischemic myocardium. This signalling system seems to be transmitted via cGMP and opposes the effects of phosphodiesterase enzymes. A similar mechanism has been suggested to contribute to the protection seen after preconditioning .In our previous experiments, the separate inhibition of the L-arginine-nitric oxide and the cyclooxygenase pathways with L-NAME and meclofenamate , respectively, markedly attenuated, but did not completely reverse, the anti-arrhythmic effects of ‘classical’ ischemic preconditioning. These studies provided indirect evidence of roles for nitric oxide and prostacyclin in the antiarrhythmic protection afforded by preconditioning in the canine heart. The present study, in which we blocked the generation of both nitric oxide and prostacyclin by simultaneously inhibiting their synthesis pathways before preconditioning, provides further evidence that both nitric oxide and prostacyclin are generated during the preconditioning stimulus and contribute to antiar-rhythmic protection. Take advantage of this opportunity – buy ventolin inhalers to enjoy lowest prices online.

In our previous experiments, the separate inhibition of the L-arginine-nitric oxide and the cyclooxygenase pathways with L-NAME and meclofenamate , respectively, markedly attenuated, but did not completely reverse, the anti-arrhythmic effects of ‘classical’ ischemic preconditioning. These studies provided indirect evidence of roles for nitric oxide and prostacyclin in the antiarrhythmic protection afforded by preconditioning in the canine heart. The present study, in which we blocked the generation of both nitric oxide and prostacyclin by simultaneously inhibiting their synthesis pathways before preconditioning, provides further evidence that both nitric oxide and prostacyclin are generated during the preconditioning stimulus and contribute to antiar-rhythmic protection.