- Title
- Central nervous integration of coronary reflexes
- Creator
- White, Saxon William; Moore, Peter G.; Gazibarich, Gary J.; Porges, William L.; Quail, Anthony W.
- Relation
- Vasodilatation: Vascular Smooth Muscle, Peptides, Autonomic Nerves, and Endothelium p. 299-306
- Publisher
- Raven Press
- Resource Type
- book chapter
- Date
- 1988
- Description
- Questions concerning the power of central nervous factors to significantly regulate coronary conductance receive new impetus each time a patient presents with unexplained chest pain. A familiar story is that of Mrs. V. C., who has bouts of crushing central chest pain at inappropriate times, as well as reproducible progressive and diagnostic ST segment depression on her electrocardiogram without pain during exercise to exhaustion, while having a normal coronary arteriogram and thallium scan. Such clinical observations suggest that some inherent mismatch during exercise can exist between neurohumoral vasconstrictor and local vasodilator factors. Furthermore, although the effects on coronary conductance of conventional experimental stimuli (i.e., those affecting arterial baro- and chemoreceptors) and of cardiac and pulmonary receptors have been investigated, the effects of direct central nervous influences (e.g., emotion) remain largely unknown. Moreover, how the gain of peripheral reflex changes in coronary conductance may be altered by central influences is also unknown. The studies summarized in this chapter were undertaken to investigate the possibility that central nervous μ-opioid agonists such as fentanyl, and monoamines such as 5-hydroxytryptamine (serotonin), can alter vagal vasodilator and sympathetic vasoconstrictor mechanisms in the coronary circulation at rest and during reflex disturbances. Further justification for such studies comes from data showing that humans and other mammals have a distribution of opiate receptors and serotonin-synthesizing neurons concentrated in and around structures known to be part of cardiorespiratory reflex pathways. Questions concerning the power of central nervous factors to significantly regulate coronary conductance receive new impetus each time a patient presents with unexplained chest pain. A familiar story is that of Mrs. V. C., who has bouts of crushing central chest pain at inappropriate times, as well as reproducible progressive and diagnostic ST segment depression on her electrocardiogram without pain during exercise to exhaustion, while having a normal coronary arteriogram and thallium scan. Such clinical observations suggest that some inherent mismatch during exercise can exist between neurohumoral vasconstrictor and local vasodilator factors. Furthermore, although the effects on coronary conductance of conventional experimental stimuli (i.e., those affecting arterial baro- and chemoreceptors) and of cardiac and pulmonary receptors have been investigated, the effects of direct central nervous influences (e.g., emotion) remain largely unknown. Moreover, how the gain of peripheral reflex changes in coronary conductance may be altered by central influences is also unknown. The studies summarized in this chapter were undertaken to investigate the possibility that central nervous μ-opioid agonists such as fentanyl, and monoamines such as 5-hydroxytryptamine (serotonin), can alter vagal vasodilator and sympathetic vasoconstrictor mechanisms in the coronary circulation at rest and during reflex disturbances. Further justification for such studies comes from data showing that humans and other mammals have a distribution of opiate receptors and serotonin-synthesizing neurons concentrated in and around structures known to be part of cardiorespiratory reflex pathways.
- Subject
- central nervous factors; cardiac; pulmonary; chest pain; coronary reflexes
- Identifier
- http://hdl.handle.net/1959.13/939152
- Identifier
- uon:12744
- Identifier
- ISBN:0881674087
- Language
- eng
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