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Evidence against the presence of ventricular chemoreceptors activated by hypoxia and hypercapnia
Journal article   Peer reviewed

Evidence against the presence of ventricular chemoreceptors activated by hypoxia and hypercapnia

Allyn L Mark, François M Abboud, Donald D Heistad, Phillip G Schmid and U. James Johannsen
The American journal of physiology, Vol.227(1), pp.178-182
07/1974
DOI: 10.1152/ajplegacy.1974.227.1.178
PMID: 4843369

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Abstract

This study was performed to test the hypothesis that the Bezold Jarisch or coronary chemoreflex is activated by hypoxia and hypercapnia. The circumflex coronary artery of 10 anesthetized dogs was perfused at constant flow with: normoxic, normocapnic blood and hypoxic, hypercapnic blood (PO2, 43 ± 3 mmHg; PCO2 > 100 mmHg; pH 6.96 ± 0.13 U) while maintaining systemic normoxia and normocapnia. Reflex vascular responses were observed in innervated, perfused gracilis muscle and hindpaw. Local coronary hypoxia and hypercapnia did not produce significant reflex vascular responses although the Bezold Jarisch reflex was intact; the hypoxic, hypercapnic blood caused coronary vasodilatation; the degree of hypoxia and hypercapnia was sufficient to activate chemoreceptors as indicated by reflex vasoconstriction in muscle when carotid chemoreceptors were exposed to the hypoxic and hypercapnic blood. Vagotomy blocked hypotension produced by coronary injection of nicotine, but not that during coronary hypoxia and hypercapnia. The results indicate that the Bezold Jarisch or coronary chemoreflex is not activated by hypoxia and hypercapnia and suggest that distal coronary vessels and myocardium do not contain receptors which have the physiologic characteristics of arterial chemoreceptors.
Hypoxia Blood Pressure Coronary Circulation Respiratory Insufficiency - etiology Male Chemoreceptor Cells - physiology Carbon Dioxide - blood Vagotomy Oxygen - blood Nicotine - pharmacology Hypercapnia Vagus Nerve - physiology Animals Dilatation Bradycardia - etiology Dogs Heart Ventricles - innervation

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