Participation of nitric oxide in regional coronary bloodflow regulation during myocardial ischemia in the canine heart (part 1)

30 Aug
2012

canine heart (part 1)

Nitric oxide participates in the regulation of coronary bloodflow during reactive hyperemia . This observation may imply that the release of nitric oxide is mediated by ischemia as a regulatory mechanism between the myocardial cell and the endothelial cell. However, it is uncertain whether the stimulus for production of nitric oxide in the endothelium during reactive hyperemia is the ischemia or the sudden increase in shear stress on the endothelium after the release of coronary occlusion. There is experimental evidence for the release of ATP from the ischemic myocardial cell and for the existence of purinergic receptors mediating the production of nitric oxide in vascular endothelial cells .Although this evidence suggests that the participation of ischemia is a stimulus for nitric oxide release in the endothelium, it is circumstantial and does not discount the possibility that hyperemia, after reopening of the vessel, is due to a sudden increase in shear stress or that both mechanisms may occur. Because shear stress is a well known stimulus for the production of nitric oxide by the endothelium , we tested the hypothesis that ischemia induces the release of nitric oxide independently of changes in shear stress. We performed experiments in dogs and measured left ventricular transmural coronary bloodflow with the microspheres technique, both in the normal myocardium and in the myocardium rendered ischemic, by decreasing the coronary perfusion pressure to a low constant value before and after inhibition of nitric oxide synthesis. You can soon shop with a nice pharmacy offering cialis super active online here to benefit more.

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