Mechanisms of hypoxic and ischemic coronary dilation

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(1)Hypoxic coronary vasodilatationWe investigated potential involvement of nitric oxide, prostacyclin, adenosine, ATP sensitive K channel-opening in coronary vasodilation during 15 minutes of hypoxia in isolated rat hearts. NO greatly contributes the maintenance of the coronary flow during normoxia (40%). However, NO production is almost completely inhibited during hypoxia. Hypoxia immediately opens the K_<ATP> channels and several minutes later enhances adenosine production, thus relaxing coronary resistant vessels. Reoxygenation also dilates coronary vasculature by opening the K_<Ca> channels.Reactive hyperemiaTo clarify factors other than NO involved in reactive hyperemia after short (30sec) and a long (300sec) coronary global no-flow ischemia in isolated rat hearts. Opening of K_<ATP> channel contributes to coronary vasodilation in reactive hyperemia after short 30-sec ischemia, and opening of K_<Ca>, but not K_<ATP> channel contributes to it after long 300-sec ischemia.