Journal
RESPIRATORY PHYSIOLOGY & NEUROBIOLOGY
Volume 156, Issue 3, Pages 241-249Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.resp.2006.11.003
Keywords
prostaglandin E-2; hyperthermia; pulmonary C-fibers; airway inflammation
Categories
Funding
- NHLBI NIH HHS [R01 HL058686, HL-67379, R01 HL067379, R56 HL067379] Funding Source: Medline
Ask authors/readers for more resources
This study was carried out to investigate whether the pulmonary C-fiber hypersensitivity induced by hyperthermia is altered by prostaglandin E-2 (PGE(2)). Single-unit afferent activities of pulmonary C-fibers were recorded in anesthetized, artificially ventilated rats when the intrathoracic temperature (T-it) was maintained at normal (N; -36 degrees C) and hyperthermia levels (N; similar to 36 degrees) by perfusion of heated saline into the thoracic chamber for 3 min. After similar to 20 min of recovery, the fiber activities were recorded again during infusion of PGE(2) at both N and H levels of T-it. Our study showed: (1) The baseline fiber activity and responses to lung inflation, right-atrial injection of capsaicin and adenosine were all increased by increasing T-it from N to H, and these hyperthermia-induced increases in sensitivities were also significantly augmented by PGE(2). (2) These enhanced sensitivities induced by PGE(2) were abolished by pretreatment with AH6809 and AH23848, selective antagonists Of EP2 and EP4 prostanoid receptors, respectively. In conclusion, the hyperthermia-induced hypersensitivity of vagal pulmonary C-fibers is potentiated by PGE(2), and this effect is mediated through activation of EP2 and EP4 prostanoid receptors. (C) 2006 Elsevier B.V. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available