Stimulatory effect of CO2 on vagal bronchopulmonary C-fiber afferents during airway inflammation.
This study investigated 1) whether pulmonary C fibers are activated by a transient increase in the CO2 concentration of alveolar gas; and 2) if the CO2 sensitivity of these afferents is altered during airway inflammation. Single-unit pulmonary C-fiber activity was recorded in anesthetized, open-chest rats. Transient alveolar hypercapnia (HPC) was induced by administering a CO2-enriched gas mixture (25-30% CO2, 21% O2, balance N2) for five to eight breaths, which increased alveolar CO2 concentration progressively to near or above 13% for 3-5 s and lowered the arterial pH transiently to 7.10 +/- 0.05. Our results showed the following. 1) HPC evoked only a mild stimulation in a small fraction (4/47) of pulmonary C fibers, and there was no significant change in fiber activity (change in fiber activity = 0.22 +/- 0.16 imp/s; P > 0.1, n = 47). 2) In sharp contrast, after airway exposure to poly-L-lysine, a cationic protein known to induce mucosal injury, the same challenge of transient HPC activated 87.5% of the pulmonary C fibers tested and evoked a distinct stimulatory effect on these afferents (change in fiber activity = 6.59 +/- 1.78 imp/s; P < 0. 01, n = 8). 3) Similar potentiation of the C-fiber response to HPC was also observed after acute exposure to ozone (n = 6) and during a constant infusion of inflammatory mediators such as adenosine (n = 15) or prostaglandin E2 (n = 12). 4) The enhanced C-fiber sensitivity to CO2 after poly-L-lysine was completely abrogated by infusion of NaHCO3 (1.82 mmol.kg(-1).min(-1)) that prevented the reduction in pH during HPC (n = 6). In conclusion, only a small percentage (<10%) of the bronchopulmonary C fibers exhibit CO2 sensitivity under control conditions, but alveolar HPC exerts a consistent and pronounced stimulatory effect on the C-fiber endings during airway inflammation. This effect of CO2 is probably mediated through the action of hydrogen ions.
Lin
Ruei-Lung
RL
Dept. of Physiology, Univ. of Kentucky Medical Center, 800 Rose St., Lexington, KY 40536-0298, USA.
Gu
Qihai
Q
Lin
You-Shuei
YS
Lee
Lu-Yuan
LY
D000138:Acidosis / Q000503:physiopathology; D000818:Animals; D016535:Bronchial Hyperreactivity / Q000503:physiopathology*; D002245:Carbon Dioxide / Q000502:physiology*; D006935:Hypercapnia / Q000503:physiopathology*; D008168:Lung / Q000294:innervation / Q000502:physiology; D008297:Male; D036421:Nerve Fibers, Unmyelinated / Q000502:physiology*; D009475:Neurons, Afferent / Q000502:physiology / Q000648:ultrastructure; D011014:Pneumonia / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020545:Respiratory Mucosa / Q000294:innervation / Q000502:physiology; D014630:Vagus Nerve / Q000166:cytology / Q000502:physiology*
D002245:Carbon Dioxide