Journal of Applied Physiology AJP: Gastrointestinal and Liver Physiology
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J Appl Physiol 94: 1987-1998, 2003. First published January 10, 2003; doi:10.1152/japplphysiol.01047.2002
8750-7587/03 $5.00
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Vol. 94, Issue 5, 1987-1998, May 2003

Afferent vagal pathways mediating respiratory reflexes evoked by ROS in the lungs of anesthetized rats

Ting Ruan1, Ching-Yin Ho1,2, and Yu Ru Kou1

1 Institute of Physiology, School of Medicine, National Yang-Ming University, and 2 Department of Otolaryngology, Taipei Veterans General Hospital, Taipei 112, Taiwan

We investigated the afferent vagal pathways mediating respiratory reflexes evoked by reactive oxygen species (ROS) in the lungs of anesthetized rats. Spontaneous inhalation of 0.2% aerosolized H2O2 acutely evoked initial bradypnea followed by delayed tachypnea, which was frequently mixed with delayed augmented inspiration. The initial response was abolished after perivagal capsaicin treatment (PCT), but was prolonged during vagal cooling (VC) to 7°C; PCT and VC are known to differentially block the conduction of unmyelinated C and myelinated fibers, respectively. The delayed responses were eliminated during VC but emerged earlier after PCT. Vagotomy, catalase (an antioxidant for H2O2), dimethylthiourea (an antioxidant for · OH), or deferoxamine (an antioxidant for · OH) largely or totally suppressed these reflexive responses, whereas sham nerve treatment, heat-inactivated catalase, saline vehicle, or iron-saturated deferoxamine failed to do so. These results suggest that 1) the H2O2-evoked initial and delayed airway reflexes are antagonistic and may result from stimulation of lung C fibers and rapidly adapting receptors, respectively, and 2) the reflex effects of H2O2 are, in part, due to the action of · OH on these afferents.

vagal sensory receptors; oxygen radicals; reactive oxygen species; hydrogen peroxide


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