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J Appl Physiol 94: 1446-1454, 2003. First published December 13, 2002; doi:10.1152/japplphysiol.00767.2002
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Vol. 94, Issue 4, 1446-1454, April 2003

Acute hypoxia prolongs the apnea induced by right atrial injection of capsaicin

Fadi Xu, Qi-Hai Gu, Tongrong Zhou, and Lu-Yuan Lee

Department of Physiology, University of Kentucky, Lexington, Kentucky 40536

Inspiratory central drive is augmented by acute hypoxia that leads to a hyperventilation, but it is inhibited by capsaicin (Cap)-induced stimulation of pulmonary C fibers (PCFs) that produces an expiratory apnea. We hypothesized that acute hypoxia should shorten or eliminate the Cap-induced apnea. The ventilatory responses to bolus injection of Cap (0.2-0.5 µg) into the right atrium before and during acute hypoxia (10% O2 for ~1 min; Hypoxia+Cap) were compared in anesthetized and spontaneously breathing rats. We found that Cap injection during acute hypoxia produced an extremely long-lasting apnea (69.67 ± 11.97 s) that was 16-fold longer than the apnea induced by Cap alone (expiratory duration = 4.37 ± 0.53 s; P < 0.01). A similar prolonged apnea was also observed during hypoxia in anesthetized guinea pigs. Bilateral vagotomy abolished apneic responses to Cap both before and during hypoxia. Subsequent recording of single-fiber activity of PCFs (PCFA) showed that acute hypoxia did not significantly affect baseline PCFA but that it doubled PCFA responses to Cap via increasing both the firing rate (3.34 ± 0.76 to 7.65 ± 1.32 impulses/s; P < 0.05) and burst duration (1.12 ± 0.18 to 2.32 ± 0.31 s; P < 0.05). These results suggest that acute hypoxia augments PCF-mediated inspiratory inhibition and thereby leads to an extremely long-lasting apnea. This interaction is partially due to hypoxic sensitization of PCF response to Cap.

pulmonary C fibers; carotid chemoreceptors; interaction; rat and guinea pig


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