There is strong evidence that during the early phase of myocardial ischemia a substantial amount of prostacyclin is released and that this determines the severity of occlusion arrhythmias . Indeed, potentiation of prostacyclin formation, for example with nafazatrom or administration of a stable prostacyclin analogue, 7-oxo-prostacyclin , results in a profound antiarrhythmic effect. On the basis of these previous studies it seemed likely that prostacyclin is also involved in the antiarrhythmic effect of ischemic preconditioning. Indeed, when the cyclooxygenase pathway was blocked with meclofenamate before preconditioning, antiarrhythmic protection was markedly attenuated . We presume that prevention of the formation of prostacyclin is one of the explanations for this loss of protection.Recently, Goulielmos and colleagues demonstrated that inhibition of prostacyclin and nitric oxide release from endothelial cells during global ischemia in guinea-pig isolated hearts accentuated the ischemia-induced reduction in 95% action potential duration and reduced the time to onset of VT. They suggested that endothelium-derived nitric oxide and prostacyclin modify arrhythmogenesis during myocardial ischemia and that this is probably mediated through changes in platelet activation. Dreaming of a reliable pharmacy that could give you an opportunity to buy any amounts of ventolin inhalers with no prescription required and spend less money?