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Coronary artery reactivity in human vessels: some questions and some answers
Insights
Coronary artery spasm, triggered by agents like acetylcholine, can significantly impair heart blood flow. This response is more pronounced in cardiac patients, suggesting multiple factors contribute to coronary artery constriction.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
Background:
- Coronary artery spasm can severely affect cardiac function by impeding blood flow.
- Human coronary arteries contract in response to acetylcholine, unlike dog vessels which relax.
Purpose of the Study:
- To investigate the constrictive effects of acetylcholine and other agents on human coronary arteries.
- To explore factors contributing to coronary artery spasm, particularly in cardiac patients.
Main Methods:
- In vitro studies on human and dog coronary artery segments.
- Assessment of contractile responses to acetylcholine, 5-hydroxytryptamine (5-HT), histamine, and norepinephrine.
- Evaluation of field stimulation and atropine's effects on coronary artery strips.
- Comparison of coronary artery reactivity and mediator content between cardiac and non-cardiac patients.
Main Results:
- Acetylcholine is a potent constrictor of human coronary arteries, comparable to 5-HT and histamine, and stronger than norepinephrine.
- Field stimulation induced vasoconstriction, partially blocked by atropine.
- Epicardial arteries from cardiac and older patients showed heightened reactivity to agonists.
- Coronary tissue from cardiac patients had increased stores of 5-HT and significantly higher histamine levels.
Conclusions:
- Acetylcholine plays a significant role in human coronary artery constriction.
- Enhanced arterial reactivity and elevated histamine levels in cardiac patients may predispose them to spasm.
- Coronary artery spasm can be initiated by various intrinsic and extrinsic factors, including autonomic nervous system activity and vasoactive substances like histamine and 5-HT.
Abstract:
Spasm of a conduit coronary artery, converting it into a major resistance vessel impeding myocardial blood flow, may have severe short- or long-term effects on cardiac rhythm and systolic ejection of blood. It is now clear that human coronary arteries in vitro contract to acetylcholine but that relaxation is the only response observed in dog coronary vessels. Acetylcholine is as powerful a constrictor of human coronary arteries, in terms of tension induced, as 5-hydroxytryptamine (5-HT) or histamine and is a substantially more powerful constrictor than norepinephrine. Field stimulation of coronary artery strips caused a vasoconstriction that was partially antagonized by atropine (3.45 X 10(-6) M). An enhanced reactivity of the epicardial arteries of cardiac and older patients to several agonists was also observed and appears to provide a background against which a number of vasoactive agents might induce spasm. Coronary tissue from cardiac patients also contains stores of 5-HT and histamine, and the histamine levels are substantially increased above the values in vessels from noncardiac patients. Coronary artery spasm or contraction probably can be initiated by diverse intrinsic and extrinsic influences, including autonomic discharge from either the parasympathetic or sympathetic nervous system or from histamine or 5-HT, and probably no one agent or entity is causative in all cases.