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Role of the carotid bodies in chemosensory ventilatory responses in the anesthetized mouse

¹Department of Physiology, Showa University School of Medicine, Tokyo 142-8555, Japan; and ²Department of Neurophysiology, Medical Research Center, Polish Academy of Sciences, Warsaw 02-106, Poland

Submitted 9 January 2004 ; accepted in final form 1 June 2004

We examined the effects of carotid body denervation on ventilatory responses to normoxia (21% O₂ in N₂ for 240 s), hypoxic hypoxia (10 and 15% O₂ in N₂ for 90 and 120 s, respectively), and hyperoxic hypercapnia (5% CO₂ in O₂ for 240 s) in the spontaneously breathing urethane-anesthetized mouse. Respiratory measurements were made with a whole body, single-chamber plethysmograph before and after cutting both carotid sinus nerves. Baseline measurements in air showed that carotid body denervation was accompanied by lower minute ventilation with a reduction in respiratory frequency. On the basis of measurements with an open-circuit system, no significant differences in O₂ consumption or CO₂ production before and after chemodenervation were found. During both levels of hypoxia, animals with intact sinus nerves had increased respiratory frequency, tidal volume, and minute ventilation; however, after chemodenervation, animals experienced a drop in respiratory frequency and ventilatory depression. Tidal volume responses during 15% hypoxia were similar before and after carotid body denervation; during 10% hypoxia in chemodenervated animals, there was a sudden increase in tidal volume with an increase in the rate of inspiration, suggesting that gasping occurred. During hyperoxic hypercapnia, ventilatory responses were lower with a smaller tidal volume after chemodenervation than before. We conclude that the carotid bodies are essential for maintaining ventilation during eupnea, hypoxia, and hypercapnia in the anesthetized mouse.

carotid sinus nerve; chemodenervation; chemoreceptor; hypoxia; hypercapnia