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J Appl Physiol (December 13, 2002). doi:10.1152/japplphysiol.00767.2002
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Articles in PresS, published online ahead of print December 13, 2002
J Appl Physiol, 10.1152/jap.00767.2002
Submitted on August 22, 2002
Accepted on December 11, 2002

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

Fadi Xu1*, Qi-Hai Gu1, Tongrong Zhou1, and Lu-Yuan Lee1

1 Department of Physiology, University of Kentucky, Lexington, KY, USA

* To whom correspondence should be addressed. E-mail: fxu{at}lrri.org.

Inspiratory central drive is augmented by acute hypoxia that leads to a hyperventilation, but 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 sec) that was 16-fold longer than the apnea induced by CAP alone (TE = 4.37 ± 0.53 sec; 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 doubled PCFA responses to CAP via increasing both the firing rate (3.34 ± 0.76 imps sec-1 to 7.65 ± 1.32 imps sec-1; P < 0.05) and burst duration (1.12 ± 0.18 sec to 2.32 ± 0.31 sec; 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.




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