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- W108584726 abstract "At the turn of the last century, Colbeck proposed that ischemic cardiac pain might be related to distention of the ventricular wall (the 'mechanical hypothesis'). Three decades later, Lewis hypothesized that ischemic pain might be elicited by the intramyocardial release of pain-producing substances induced by ischemia ('chemical hypothesis'). Studies carried out in the past 10 years have given strong support to the chemical hypothesis, as they have consistently shown that adenosine is a mediator of ischemic cardiac pain. Adenosine-induced ischemic cardiac pain is mainly mediated by stimulation of A1 receptors located in cardiac nerve endings and is potentiated by substance P. Conversely, the magnitude and rate of left ventricular dilatation during ischemia do not predict the severity of angina. It is worth noting, however, that stretching of epicardial coronary arteries may cause angina in the absence of myocardial ischemia. & Heart Metab. 2004;24:5-7." @default.
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- W108584726 date "2004-01-01" @default.
- W108584726 modified "2023-09-27" @default.
- W108584726 title "Molecular mechanisms of cardiac ischemic pain" @default.
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