Direct effects of inhaled nitric oxide on canine peripheral airways

Karen Sue Lindeman, A. Aryana, C. A. Hirshman

Research output: Contribution to journalArticle

Abstract

The effects of nitric oxide on peripheral airways in vivo, and whether these effects occur via direct or indirect mechanisms, are unknown. We studied effects of inhaled nitric oxide on histamine-constricted canine peripheral airways in the presence or absence of atropine and an inhibitor of guanylyl cyclase, methylene blue. Peripheral resistance (Rp) was measured by using a wedged-bronchoscope technique in anesthetized dogs. A stable baseline Rp was established. Histamine was infused intravenously, and increasing concentrations of nitric oxide (50-500 ppm) were delivered through the bronchoscope. In separate experiments, histamine was infused intravenously in the presence or absence of atropine (0.2 mg/kg iv) or methylene blue (20 mg/min iv). When Rp stabilized, nitric oxide (500 ppm) was delivered. Nitric oxide partially reversed histamine-induced bronchoconstriction in a dose- dependent fashion (maximum of 42 ± 3% reduction at 500 ppm; n = 5; P <0.01) that did not differ in the presence or absence of atropine. Methylene blue blocked the effect of nitric oxide on histamine-induced constriction (n = 6; P = 0.45). These findings suggest that high concentrations of nitric oxide produce small but significant bronchodilation of peripheral airways through a mechanism independent of the cholinergic neural pathway. The mechanism of action appears to involve activation of guanylyl cyclase.

Original languageEnglish (US)
Pages (from-to)1898-1903
Number of pages6
JournalJournal of Applied Physiology
Volume78
Issue number5
StatePublished - 1995

Fingerprint

Canidae
Nitric Oxide
Histamine
Methylene Blue
Atropine
Bronchoscopes
Guanylate Cyclase
Neural Pathways
Bronchoconstriction
Constriction
Vascular Resistance
Cholinergic Agents
Dogs

Keywords

  • albuterol
  • bronchoconstriction
  • collateral resistance
  • histamine
  • methylene blue
  • nitrogen dioxide

ASJC Scopus subject areas

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

Cite this

Direct effects of inhaled nitric oxide on canine peripheral airways. / Lindeman, Karen Sue; Aryana, A.; Hirshman, C. A.

In: Journal of Applied Physiology, Vol. 78, No. 5, 1995, p. 1898-1903.

Research output: Contribution to journalArticle

Lindeman, Karen Sue ; Aryana, A. ; Hirshman, C. A. / Direct effects of inhaled nitric oxide on canine peripheral airways. In: Journal of Applied Physiology. 1995 ; Vol. 78, No. 5. pp. 1898-1903.
@article{701c6f440d9b4d5aaa8d99dfc1aa07e2,
title = "Direct effects of inhaled nitric oxide on canine peripheral airways",
abstract = "The effects of nitric oxide on peripheral airways in vivo, and whether these effects occur via direct or indirect mechanisms, are unknown. We studied effects of inhaled nitric oxide on histamine-constricted canine peripheral airways in the presence or absence of atropine and an inhibitor of guanylyl cyclase, methylene blue. Peripheral resistance (Rp) was measured by using a wedged-bronchoscope technique in anesthetized dogs. A stable baseline Rp was established. Histamine was infused intravenously, and increasing concentrations of nitric oxide (50-500 ppm) were delivered through the bronchoscope. In separate experiments, histamine was infused intravenously in the presence or absence of atropine (0.2 mg/kg iv) or methylene blue (20 mg/min iv). When Rp stabilized, nitric oxide (500 ppm) was delivered. Nitric oxide partially reversed histamine-induced bronchoconstriction in a dose- dependent fashion (maximum of 42 ± 3{\%} reduction at 500 ppm; n = 5; P <0.01) that did not differ in the presence or absence of atropine. Methylene blue blocked the effect of nitric oxide on histamine-induced constriction (n = 6; P = 0.45). These findings suggest that high concentrations of nitric oxide produce small but significant bronchodilation of peripheral airways through a mechanism independent of the cholinergic neural pathway. The mechanism of action appears to involve activation of guanylyl cyclase.",
keywords = "albuterol, bronchoconstriction, collateral resistance, histamine, methylene blue, nitrogen dioxide",
author = "Lindeman, {Karen Sue} and A. Aryana and Hirshman, {C. A.}",
year = "1995",
language = "English (US)",
volume = "78",
pages = "1898--1903",
journal = "Journal of Applied Physiology",
issn = "0161-7567",
publisher = "American Physiological Society",
number = "5",

}

TY - JOUR

T1 - Direct effects of inhaled nitric oxide on canine peripheral airways

AU - Lindeman, Karen Sue

AU - Aryana, A.

AU - Hirshman, C. A.

PY - 1995

Y1 - 1995

N2 - The effects of nitric oxide on peripheral airways in vivo, and whether these effects occur via direct or indirect mechanisms, are unknown. We studied effects of inhaled nitric oxide on histamine-constricted canine peripheral airways in the presence or absence of atropine and an inhibitor of guanylyl cyclase, methylene blue. Peripheral resistance (Rp) was measured by using a wedged-bronchoscope technique in anesthetized dogs. A stable baseline Rp was established. Histamine was infused intravenously, and increasing concentrations of nitric oxide (50-500 ppm) were delivered through the bronchoscope. In separate experiments, histamine was infused intravenously in the presence or absence of atropine (0.2 mg/kg iv) or methylene blue (20 mg/min iv). When Rp stabilized, nitric oxide (500 ppm) was delivered. Nitric oxide partially reversed histamine-induced bronchoconstriction in a dose- dependent fashion (maximum of 42 ± 3% reduction at 500 ppm; n = 5; P <0.01) that did not differ in the presence or absence of atropine. Methylene blue blocked the effect of nitric oxide on histamine-induced constriction (n = 6; P = 0.45). These findings suggest that high concentrations of nitric oxide produce small but significant bronchodilation of peripheral airways through a mechanism independent of the cholinergic neural pathway. The mechanism of action appears to involve activation of guanylyl cyclase.

AB - The effects of nitric oxide on peripheral airways in vivo, and whether these effects occur via direct or indirect mechanisms, are unknown. We studied effects of inhaled nitric oxide on histamine-constricted canine peripheral airways in the presence or absence of atropine and an inhibitor of guanylyl cyclase, methylene blue. Peripheral resistance (Rp) was measured by using a wedged-bronchoscope technique in anesthetized dogs. A stable baseline Rp was established. Histamine was infused intravenously, and increasing concentrations of nitric oxide (50-500 ppm) were delivered through the bronchoscope. In separate experiments, histamine was infused intravenously in the presence or absence of atropine (0.2 mg/kg iv) or methylene blue (20 mg/min iv). When Rp stabilized, nitric oxide (500 ppm) was delivered. Nitric oxide partially reversed histamine-induced bronchoconstriction in a dose- dependent fashion (maximum of 42 ± 3% reduction at 500 ppm; n = 5; P <0.01) that did not differ in the presence or absence of atropine. Methylene blue blocked the effect of nitric oxide on histamine-induced constriction (n = 6; P = 0.45). These findings suggest that high concentrations of nitric oxide produce small but significant bronchodilation of peripheral airways through a mechanism independent of the cholinergic neural pathway. The mechanism of action appears to involve activation of guanylyl cyclase.

KW - albuterol

KW - bronchoconstriction

KW - collateral resistance

KW - histamine

KW - methylene blue

KW - nitrogen dioxide

UR - http://www.scopus.com/inward/record.url?scp=0028998194&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028998194&partnerID=8YFLogxK

M3 - Article

C2 - 7649928

AN - SCOPUS:0028998194

VL - 78

SP - 1898

EP - 1903

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 0161-7567

IS - 5

ER -