Simultaneous blockade of the cyclooxygenase and L-arginine-nitric oxide pathways prevents the antiarrhythmic effects of classical preconditioning (part 14)

classical preconditioning (part 14)

A variety of potentially protective mediators might be released under conditions of myocardial ischemia . These include adenosine, prostacyclin, bradykinin and nitric oxide; each of these may be considered as an endogenous cardioprotective substance . Indeed, there is good evidence that nitric oxide is released into the coronary circulation under both basal and stimulated conditions and that, through the elevation of cGMP, it regulates the coronary circulation. The suggestion that nitric oxide might be involved in the antiarrhythmic effects of ischemic preconditioning in the canine came first from studies in which the generation of nitric oxide or its effect on soluble guanylyl cyclase were prevented by either L-NAME or methylene blue , respectively. In contrast, L-NAME failed to reverse the anti-arrhythmic effect of preconditioning in rats , and there is even some evidence that L-NAME reduces, rather than increases, infarct size in rabbit isolated hearts via an adenosine-dependent mechanism. Although we have no direct evidence for the hypothesis that nitric oxide plays a mediator role in preconditioning (nitric oxide levels were not measured in these particular experiments), a number of studies support the concept that nitric oxide is an important endogenous cardioprotective substance under conditions of ischemia and reperfusion. Recently, Pabla and Curtis demonstrated that nitric oxide protected against VF in rat hearts during reperfusion following prolonged ischemia. Shop online with the best pharmacy that will ensure high quality of your medications and will offer cheapest proventil inhaler dosage with no rx required any time you need this or any other one for your medical problem.

Category: Cardiology

Tags: Cyclooxygenase pathway, Ischemic preconditioning, L-arginine-nitric oxide pathway

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