A β2-adrenergic agonist inhibits dry air-induced injury in canine peripheral airways

C. Omori, B. H. Schofield, Wayne A Mitzner, A. N. Freed

Research output: Contribution to journalArticle

Abstract

We examined the effects of β2-agonist on dry air-induced injury in canine peripheral airways. Dry air-induced bronchoconstriction (AIB) was assessed by measuring peripheral airway resistance in anesthetized dogs. Salbutamol reduced AIB by ~75% compared with control values. Colloidal carbon was used to detect bronchovascular leakage in contralateral sublobar segments that were pretreated with saline or salbutamol. About 87% of the perimeter of bronchi was damaged after dry air challenge in saline-treated segments. Salbutamol reduced mucosal damage by ~30% (P <0.05). The mucosa of bronchioles was not injured. The average goblet-to-ciliated cell ratio (which reflects mucosal perturbation) in bronchi decreased from 0.38 in control bronchi to 0.15 in challenged bronchi, and this effect was also evident in bronchioles. Salbutamol did not affect this decrement. Dry air challenge also caused degranulation of mast cells located below damaged mucosa, dilation of bronchial vessels, and leakage from capillaries and venules located below normal ciliated and damaged mucosa of bronchi. Thus, we conclude that salbutamol attenuates epithelial damage and AIB but fails to inhibit mast cell degranulation and vascular hyperpermeability.

Original languageEnglish (US)
Pages (from-to)2169-2179
Number of pages11
JournalJournal of Applied Physiology
Volume78
Issue number6
StatePublished - 1995

Fingerprint

Adrenergic Agonists
Albuterol
Bronchi
Canidae
Air
Bronchoconstriction
Wounds and Injuries
Bronchioles
Mucous Membrane
Mast Cells
Cell Degranulation
Airway Resistance
Venules
Vascular Resistance
Blood Vessels
Dilatation
Carbon
Dogs

Keywords

  • β-adrenoreceptor agonist
  • asthma
  • bronchial circulation
  • bronchovascular leakage
  • lung injury
  • mast cells

ASJC Scopus subject areas

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

Cite this

A β2-adrenergic agonist inhibits dry air-induced injury in canine peripheral airways. / Omori, C.; Schofield, B. H.; Mitzner, Wayne A; Freed, A. N.

In: Journal of Applied Physiology, Vol. 78, No. 6, 1995, p. 2169-2179.

Research output: Contribution to journalArticle

Omori, C. ; Schofield, B. H. ; Mitzner, Wayne A ; Freed, A. N. / A β2-adrenergic agonist inhibits dry air-induced injury in canine peripheral airways. In: Journal of Applied Physiology. 1995 ; Vol. 78, No. 6. pp. 2169-2179.
@article{f6c19502873e46149c76238814959729,
title = "A β2-adrenergic agonist inhibits dry air-induced injury in canine peripheral airways",
abstract = "We examined the effects of β2-agonist on dry air-induced injury in canine peripheral airways. Dry air-induced bronchoconstriction (AIB) was assessed by measuring peripheral airway resistance in anesthetized dogs. Salbutamol reduced AIB by ~75{\%} compared with control values. Colloidal carbon was used to detect bronchovascular leakage in contralateral sublobar segments that were pretreated with saline or salbutamol. About 87{\%} of the perimeter of bronchi was damaged after dry air challenge in saline-treated segments. Salbutamol reduced mucosal damage by ~30{\%} (P <0.05). The mucosa of bronchioles was not injured. The average goblet-to-ciliated cell ratio (which reflects mucosal perturbation) in bronchi decreased from 0.38 in control bronchi to 0.15 in challenged bronchi, and this effect was also evident in bronchioles. Salbutamol did not affect this decrement. Dry air challenge also caused degranulation of mast cells located below damaged mucosa, dilation of bronchial vessels, and leakage from capillaries and venules located below normal ciliated and damaged mucosa of bronchi. Thus, we conclude that salbutamol attenuates epithelial damage and AIB but fails to inhibit mast cell degranulation and vascular hyperpermeability.",
keywords = "β-adrenoreceptor agonist, asthma, bronchial circulation, bronchovascular leakage, lung injury, mast cells",
author = "C. Omori and Schofield, {B. H.} and Mitzner, {Wayne A} and Freed, {A. N.}",
year = "1995",
language = "English (US)",
volume = "78",
pages = "2169--2179",
journal = "Journal of Applied Physiology",
issn = "0161-7567",
publisher = "American Physiological Society",
number = "6",

}

TY - JOUR

T1 - A β2-adrenergic agonist inhibits dry air-induced injury in canine peripheral airways

AU - Omori, C.

AU - Schofield, B. H.

AU - Mitzner, Wayne A

AU - Freed, A. N.

PY - 1995

Y1 - 1995

N2 - We examined the effects of β2-agonist on dry air-induced injury in canine peripheral airways. Dry air-induced bronchoconstriction (AIB) was assessed by measuring peripheral airway resistance in anesthetized dogs. Salbutamol reduced AIB by ~75% compared with control values. Colloidal carbon was used to detect bronchovascular leakage in contralateral sublobar segments that were pretreated with saline or salbutamol. About 87% of the perimeter of bronchi was damaged after dry air challenge in saline-treated segments. Salbutamol reduced mucosal damage by ~30% (P <0.05). The mucosa of bronchioles was not injured. The average goblet-to-ciliated cell ratio (which reflects mucosal perturbation) in bronchi decreased from 0.38 in control bronchi to 0.15 in challenged bronchi, and this effect was also evident in bronchioles. Salbutamol did not affect this decrement. Dry air challenge also caused degranulation of mast cells located below damaged mucosa, dilation of bronchial vessels, and leakage from capillaries and venules located below normal ciliated and damaged mucosa of bronchi. Thus, we conclude that salbutamol attenuates epithelial damage and AIB but fails to inhibit mast cell degranulation and vascular hyperpermeability.

AB - We examined the effects of β2-agonist on dry air-induced injury in canine peripheral airways. Dry air-induced bronchoconstriction (AIB) was assessed by measuring peripheral airway resistance in anesthetized dogs. Salbutamol reduced AIB by ~75% compared with control values. Colloidal carbon was used to detect bronchovascular leakage in contralateral sublobar segments that were pretreated with saline or salbutamol. About 87% of the perimeter of bronchi was damaged after dry air challenge in saline-treated segments. Salbutamol reduced mucosal damage by ~30% (P <0.05). The mucosa of bronchioles was not injured. The average goblet-to-ciliated cell ratio (which reflects mucosal perturbation) in bronchi decreased from 0.38 in control bronchi to 0.15 in challenged bronchi, and this effect was also evident in bronchioles. Salbutamol did not affect this decrement. Dry air challenge also caused degranulation of mast cells located below damaged mucosa, dilation of bronchial vessels, and leakage from capillaries and venules located below normal ciliated and damaged mucosa of bronchi. Thus, we conclude that salbutamol attenuates epithelial damage and AIB but fails to inhibit mast cell degranulation and vascular hyperpermeability.

KW - β-adrenoreceptor agonist

KW - asthma

KW - bronchial circulation

KW - bronchovascular leakage

KW - lung injury

KW - mast cells

UR - http://www.scopus.com/inward/record.url?scp=0029068109&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029068109&partnerID=8YFLogxK

M3 - Article

C2 - 7665414

AN - SCOPUS:0029068109

VL - 78

SP - 2169

EP - 2179

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 0161-7567

IS - 6

ER -