Hyperoxia prevents hypoxia-induced bronchial hyperreactivity via a cyclooxygenase-independent mechanism

J. D'Brot, T. Ahmed

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

We tested the hypothesis that prior exposure to alveolar hyperoxia prevents the hypoxia-induced enhancement of bronchial reactivity, possibly via a cyclooxygenase-dependent mechanism. In 15 sheep, specific lung resistance (sRL) was measured before and after 30 min of exposure to either air or a hypoxic gas mixture (13% O2). The sheep then inhaled 50 breaths of aerosolized 5% histamine solution (n = 9) or 10 breaths of 2.5% carbachol solution (n = 9), and measurements of sRL were repeated. On subsequent days the above protocols were repeated after a 30-min exposure to hyperoxia (O2 ≥ 95%), without or after pretreatment with indomethacin (2 mg/kg). After airsham exposure, carbachol and histamine increased mean sRL to 370 ± 40 (SE) and 309 ± 65% of baseline, respectively. Exposure to the hypoxic gas mixture had no effect on baseline sRL but enhanced the airway responsiveness to carbachol and histamine; mean sRL increased to 740 ± 104 and 544 ± 76% of baseline, respectively (P < 0.05). Prior 30-min exposure to hyperoxia prevented the hypoxia-induced enhancement of bronchial reactivity to carbachol (sRL = 416 ± 66% of baseline) and histamine (sRL = 292 ± 41% of baseline) without affecting the airway responsiveness to these agents after air. Pretreatment with indomethacin did not reverse the protective effects of hyperoxia or the hypoxia-induced enhancement of bronchial reactivity. We conclude that 1) prior exposure to alveolar hyperoxia prevents the hypoxia-induced enhancement of bronchial reactivity and 2) neither the protective effects of hyperoxia nor the hypoxia-induced enhancement of bronchial reactivity is mediated via a cyclooxygenase-dependent mechanism.

Original languageEnglish
Pages (from-to)740-747
Number of pages8
JournalJournal of Applied Physiology
Volume70
Issue number2
StatePublished - Jan 1 1991
Externally publishedYes

Fingerprint

Bronchial Hyperreactivity
Hyperoxia
Prostaglandin-Endoperoxide Synthases
Carbachol
Histamine
Indomethacin
Sheep
Air
Hypoxia
Lung

Keywords

  • cyclooxygenase metabolites
  • indomethacin

ASJC Scopus subject areas

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

Cite this

Hyperoxia prevents hypoxia-induced bronchial hyperreactivity via a cyclooxygenase-independent mechanism. / D'Brot, J.; Ahmed, T.

In: Journal of Applied Physiology, Vol. 70, No. 2, 01.01.1991, p. 740-747.

Research output: Contribution to journalArticle

@article{3698773b76774ebab4c2622147105c50,
title = "Hyperoxia prevents hypoxia-induced bronchial hyperreactivity via a cyclooxygenase-independent mechanism",
abstract = "We tested the hypothesis that prior exposure to alveolar hyperoxia prevents the hypoxia-induced enhancement of bronchial reactivity, possibly via a cyclooxygenase-dependent mechanism. In 15 sheep, specific lung resistance (sRL) was measured before and after 30 min of exposure to either air or a hypoxic gas mixture (13{\%} O2). The sheep then inhaled 50 breaths of aerosolized 5{\%} histamine solution (n = 9) or 10 breaths of 2.5{\%} carbachol solution (n = 9), and measurements of sRL were repeated. On subsequent days the above protocols were repeated after a 30-min exposure to hyperoxia (O2 ≥ 95{\%}), without or after pretreatment with indomethacin (2 mg/kg). After airsham exposure, carbachol and histamine increased mean sRL to 370 ± 40 (SE) and 309 ± 65{\%} of baseline, respectively. Exposure to the hypoxic gas mixture had no effect on baseline sRL but enhanced the airway responsiveness to carbachol and histamine; mean sRL increased to 740 ± 104 and 544 ± 76{\%} of baseline, respectively (P < 0.05). Prior 30-min exposure to hyperoxia prevented the hypoxia-induced enhancement of bronchial reactivity to carbachol (sRL = 416 ± 66{\%} of baseline) and histamine (sRL = 292 ± 41{\%} of baseline) without affecting the airway responsiveness to these agents after air. Pretreatment with indomethacin did not reverse the protective effects of hyperoxia or the hypoxia-induced enhancement of bronchial reactivity. We conclude that 1) prior exposure to alveolar hyperoxia prevents the hypoxia-induced enhancement of bronchial reactivity and 2) neither the protective effects of hyperoxia nor the hypoxia-induced enhancement of bronchial reactivity is mediated via a cyclooxygenase-dependent mechanism.",
keywords = "cyclooxygenase metabolites, indomethacin",
author = "J. D'Brot and T. Ahmed",
year = "1991",
month = "1",
day = "1",
language = "English",
volume = "70",
pages = "740--747",
journal = "Journal of Applied Physiology",
issn = "8750-7587",
publisher = "American Physiological Society",
number = "2",

}

TY - JOUR

T1 - Hyperoxia prevents hypoxia-induced bronchial hyperreactivity via a cyclooxygenase-independent mechanism

AU - D'Brot, J.

AU - Ahmed, T.

PY - 1991/1/1

Y1 - 1991/1/1

N2 - We tested the hypothesis that prior exposure to alveolar hyperoxia prevents the hypoxia-induced enhancement of bronchial reactivity, possibly via a cyclooxygenase-dependent mechanism. In 15 sheep, specific lung resistance (sRL) was measured before and after 30 min of exposure to either air or a hypoxic gas mixture (13% O2). The sheep then inhaled 50 breaths of aerosolized 5% histamine solution (n = 9) or 10 breaths of 2.5% carbachol solution (n = 9), and measurements of sRL were repeated. On subsequent days the above protocols were repeated after a 30-min exposure to hyperoxia (O2 ≥ 95%), without or after pretreatment with indomethacin (2 mg/kg). After airsham exposure, carbachol and histamine increased mean sRL to 370 ± 40 (SE) and 309 ± 65% of baseline, respectively. Exposure to the hypoxic gas mixture had no effect on baseline sRL but enhanced the airway responsiveness to carbachol and histamine; mean sRL increased to 740 ± 104 and 544 ± 76% of baseline, respectively (P < 0.05). Prior 30-min exposure to hyperoxia prevented the hypoxia-induced enhancement of bronchial reactivity to carbachol (sRL = 416 ± 66% of baseline) and histamine (sRL = 292 ± 41% of baseline) without affecting the airway responsiveness to these agents after air. Pretreatment with indomethacin did not reverse the protective effects of hyperoxia or the hypoxia-induced enhancement of bronchial reactivity. We conclude that 1) prior exposure to alveolar hyperoxia prevents the hypoxia-induced enhancement of bronchial reactivity and 2) neither the protective effects of hyperoxia nor the hypoxia-induced enhancement of bronchial reactivity is mediated via a cyclooxygenase-dependent mechanism.

AB - We tested the hypothesis that prior exposure to alveolar hyperoxia prevents the hypoxia-induced enhancement of bronchial reactivity, possibly via a cyclooxygenase-dependent mechanism. In 15 sheep, specific lung resistance (sRL) was measured before and after 30 min of exposure to either air or a hypoxic gas mixture (13% O2). The sheep then inhaled 50 breaths of aerosolized 5% histamine solution (n = 9) or 10 breaths of 2.5% carbachol solution (n = 9), and measurements of sRL were repeated. On subsequent days the above protocols were repeated after a 30-min exposure to hyperoxia (O2 ≥ 95%), without or after pretreatment with indomethacin (2 mg/kg). After airsham exposure, carbachol and histamine increased mean sRL to 370 ± 40 (SE) and 309 ± 65% of baseline, respectively. Exposure to the hypoxic gas mixture had no effect on baseline sRL but enhanced the airway responsiveness to carbachol and histamine; mean sRL increased to 740 ± 104 and 544 ± 76% of baseline, respectively (P < 0.05). Prior 30-min exposure to hyperoxia prevented the hypoxia-induced enhancement of bronchial reactivity to carbachol (sRL = 416 ± 66% of baseline) and histamine (sRL = 292 ± 41% of baseline) without affecting the airway responsiveness to these agents after air. Pretreatment with indomethacin did not reverse the protective effects of hyperoxia or the hypoxia-induced enhancement of bronchial reactivity. We conclude that 1) prior exposure to alveolar hyperoxia prevents the hypoxia-induced enhancement of bronchial reactivity and 2) neither the protective effects of hyperoxia nor the hypoxia-induced enhancement of bronchial reactivity is mediated via a cyclooxygenase-dependent mechanism.

KW - cyclooxygenase metabolites

KW - indomethacin

UR - http://www.scopus.com/inward/record.url?scp=0026082982&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026082982&partnerID=8YFLogxK

M3 - Article

C2 - 1902458

AN - SCOPUS:0026082982

VL - 70

SP - 740

EP - 747

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 8750-7587

IS - 2

ER -