Abstract
Sensory innervation of the heart seems capable of perceiving the occurrence of transient myocardial ischemia. As a result, neural reflexes and pain can originate from the heart. However, while the link existing between myocardial ischemia and pain is elusive [1], as nonpainful episodes are a common clinical and experimental feature, complex cardiovascular reflexes seem to accompany experimental occlusion of a coronary artery [2–4] and transient myocardial ischemia in humans [5, 6]. Their consequences range from simple changes in heart rate and arterial pressure to the precipitation of malignant arrhythmias [7, 8]. Two hypotheses have been advanced to explain the independence of neural reflexes from pain: 1) Two sets of different afferent fibers could be responsible for mediating neural reflexes and pain, with the latter arising only concomitantly with the recruitment of high-threshold cardiac nociceptors, specifically devoted to signaling tissue damage [9]; 2) the same population of low-threshold afferent fibers would transmit different impulse codes, giving rise, respectively, to cardiovascular reflexes and pain [1].
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Montano, N., Gnecchi-Ruscone, T., Lombardi, F., Malliani, A. (1995). Excitatory Effect of Adenosine on Cardiac Sympathetic Afferent Fibers. In: Belardinelli, L., Pelleg, A. (eds) Adenosine and Adenine Nucleotides: From Molecular Biology to Integrative Physiology. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2011-5_35
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DOI: https://doi.org/10.1007/978-1-4615-2011-5_35
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