Stimulatory effect of CO2 on vagal bronchopulmonary C-fiber afferents during airway inflammation

Ruei Lung Lin, Qihai Gu, You Sfauei Lin, Lu Yuan Lee

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

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 E 2 (n = 12). 4) The enhanced C-fiber sensitivity to CO2 after poly-L-lysine was completely abrogated by infusion of NaHCO3 (1.82 mol · kg-1 · min-1) that prevented the reduction in pH during HPC (n = 6). In conclusion, only a small percentage (2 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.

Original languageEnglish
Pages (from-to)1704-1711
Number of pages8
JournalJournal of Applied Physiology
Volume99
Issue number5
DOIs
Publication statusPublished - Nov 2005
Externally publishedYes

Fingerprint

Unmyelinated Nerve Fibers
Hypercapnia
Inflammation
Lung
Lysine
Gases
Ozone
Prostaglandins E
Adenosine
Protons
Thorax
Wounds and Injuries

Keywords

  • Airway hyperreactivity
  • Airway mucosal injury
  • Hydrogen ion
  • Hypercapnia

ASJC Scopus subject areas

  • Physiology
  • Endocrinology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Stimulatory effect of CO2 on vagal bronchopulmonary C-fiber afferents during airway inflammation. / Lin, Ruei Lung; Gu, Qihai; Lin, You Sfauei; Lee, Lu Yuan.

In: Journal of Applied Physiology, Vol. 99, No. 5, 11.2005, p. 1704-1711.

Research output: Contribution to journalArticle

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abstract = "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 E 2 (n = 12). 4) The enhanced C-fiber sensitivity to CO2 after poly-L-lysine was completely abrogated by infusion of NaHCO3 (1.82 mol · kg-1 · min-1) that prevented the reduction in pH during HPC (n = 6). In conclusion, only a small percentage (2 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.",
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