Effect of furosemide on hyperpnea-induced airway obstruction, injury, and microvascular leakage

Arthur N. Freed, Varsha Surendranath Taskar, Brian Schofield, Chiharu Omori

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Furosemide attenuates hyperpnea-induced airway obstruction (HIAO) in asthmatic subjects via unknown mechanism(s). We studied the effect of furosemide on dry air-induced bronchoconstriction, mucosal injury, and bronchovascular hyperpermeability in a canine model of exercise-induced asthma. Peripheral airway resistance (Rp) was recorded before and after a 2- min dry-air challenge (DAC) at 2,000 ml/min. After pretreatment with aerosolized saline containing 0.75% dimethyl sulfoxide, DAC increased Rp 72 ± 11% (SE, n = 7) above baseline; aerosolized furosemide (10-3 M) reduced this response by ~50 ± 6% (P < 0.01). To assess bronchovascular permeability, colloidal carbon was injected (1 ml/kg iv) 1 min before DAC, and after 1 h, the vehicle- and furosemide-treated airways were prepared for morphometric analysis. Light microscopy confirmed previous studies showing that DAC damaged the airway epithelium and enhanced bronchovascular permeability. Furosemide did not inhibit dry air-induced mucosal injury or bronchovascular hyperpermeability and in fact tended to increase airway damage and vascular leakage. This positive trend toward enhanced bronchovascular permeability in DAC canine peripheral airways is consistent with the hypothesis that furosemide inhibits HIAO in part by enhancing microvascular leakage and thus counterbalancing the evaporative water loss that occurs during hyperpnea.

Original languageEnglish (US)
Pages (from-to)2461-2467
Number of pages7
JournalJournal of Applied Physiology
Volume81
Issue number6
DOIs
StatePublished - Jan 1 1996
Externally publishedYes

Fingerprint

Furosemide
Airway Obstruction
Air
Wounds and Injuries
Permeability
Canidae
Exercise-Induced Asthma
Airway Resistance
Bronchoconstriction
Dimethyl Sulfoxide
Vascular Resistance
Blood Vessels
Microscopy
Carbon
Epithelium
Light
Water

Keywords

  • asthma
  • bronchovascular permeability
  • goblet cells
  • hyperpnea-induced bronchoconstriction
  • mast cells

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Effect of furosemide on hyperpnea-induced airway obstruction, injury, and microvascular leakage. / Freed, Arthur N.; Taskar, Varsha Surendranath; Schofield, Brian; Omori, Chiharu.

In: Journal of Applied Physiology, Vol. 81, No. 6, 01.01.1996, p. 2461-2467.

Research output: Contribution to journalArticle

@article{1b3c76d6983741389cad5fc453c34a54,
title = "Effect of furosemide on hyperpnea-induced airway obstruction, injury, and microvascular leakage",
abstract = "Furosemide attenuates hyperpnea-induced airway obstruction (HIAO) in asthmatic subjects via unknown mechanism(s). We studied the effect of furosemide on dry air-induced bronchoconstriction, mucosal injury, and bronchovascular hyperpermeability in a canine model of exercise-induced asthma. Peripheral airway resistance (Rp) was recorded before and after a 2- min dry-air challenge (DAC) at 2,000 ml/min. After pretreatment with aerosolized saline containing 0.75{\%} dimethyl sulfoxide, DAC increased Rp 72 ± 11{\%} (SE, n = 7) above baseline; aerosolized furosemide (10-3 M) reduced this response by ~50 ± 6{\%} (P < 0.01). To assess bronchovascular permeability, colloidal carbon was injected (1 ml/kg iv) 1 min before DAC, and after 1 h, the vehicle- and furosemide-treated airways were prepared for morphometric analysis. Light microscopy confirmed previous studies showing that DAC damaged the airway epithelium and enhanced bronchovascular permeability. Furosemide did not inhibit dry air-induced mucosal injury or bronchovascular hyperpermeability and in fact tended to increase airway damage and vascular leakage. This positive trend toward enhanced bronchovascular permeability in DAC canine peripheral airways is consistent with the hypothesis that furosemide inhibits HIAO in part by enhancing microvascular leakage and thus counterbalancing the evaporative water loss that occurs during hyperpnea.",
keywords = "asthma, bronchovascular permeability, goblet cells, hyperpnea-induced bronchoconstriction, mast cells",
author = "Freed, {Arthur N.} and Taskar, {Varsha Surendranath} and Brian Schofield and Chiharu Omori",
year = "1996",
month = "1",
day = "1",
doi = "10.1152/jappl.1996.81.6.2461",
language = "English (US)",
volume = "81",
pages = "2461--2467",
journal = "Journal of Applied Physiology Respiratory Environmental and Exercise Physiology",
issn = "8750-7587",
publisher = "American Physiological Society",
number = "6",

}

TY - JOUR

T1 - Effect of furosemide on hyperpnea-induced airway obstruction, injury, and microvascular leakage

AU - Freed, Arthur N.

AU - Taskar, Varsha Surendranath

AU - Schofield, Brian

AU - Omori, Chiharu

PY - 1996/1/1

Y1 - 1996/1/1

N2 - Furosemide attenuates hyperpnea-induced airway obstruction (HIAO) in asthmatic subjects via unknown mechanism(s). We studied the effect of furosemide on dry air-induced bronchoconstriction, mucosal injury, and bronchovascular hyperpermeability in a canine model of exercise-induced asthma. Peripheral airway resistance (Rp) was recorded before and after a 2- min dry-air challenge (DAC) at 2,000 ml/min. After pretreatment with aerosolized saline containing 0.75% dimethyl sulfoxide, DAC increased Rp 72 ± 11% (SE, n = 7) above baseline; aerosolized furosemide (10-3 M) reduced this response by ~50 ± 6% (P < 0.01). To assess bronchovascular permeability, colloidal carbon was injected (1 ml/kg iv) 1 min before DAC, and after 1 h, the vehicle- and furosemide-treated airways were prepared for morphometric analysis. Light microscopy confirmed previous studies showing that DAC damaged the airway epithelium and enhanced bronchovascular permeability. Furosemide did not inhibit dry air-induced mucosal injury or bronchovascular hyperpermeability and in fact tended to increase airway damage and vascular leakage. This positive trend toward enhanced bronchovascular permeability in DAC canine peripheral airways is consistent with the hypothesis that furosemide inhibits HIAO in part by enhancing microvascular leakage and thus counterbalancing the evaporative water loss that occurs during hyperpnea.

AB - Furosemide attenuates hyperpnea-induced airway obstruction (HIAO) in asthmatic subjects via unknown mechanism(s). We studied the effect of furosemide on dry air-induced bronchoconstriction, mucosal injury, and bronchovascular hyperpermeability in a canine model of exercise-induced asthma. Peripheral airway resistance (Rp) was recorded before and after a 2- min dry-air challenge (DAC) at 2,000 ml/min. After pretreatment with aerosolized saline containing 0.75% dimethyl sulfoxide, DAC increased Rp 72 ± 11% (SE, n = 7) above baseline; aerosolized furosemide (10-3 M) reduced this response by ~50 ± 6% (P < 0.01). To assess bronchovascular permeability, colloidal carbon was injected (1 ml/kg iv) 1 min before DAC, and after 1 h, the vehicle- and furosemide-treated airways were prepared for morphometric analysis. Light microscopy confirmed previous studies showing that DAC damaged the airway epithelium and enhanced bronchovascular permeability. Furosemide did not inhibit dry air-induced mucosal injury or bronchovascular hyperpermeability and in fact tended to increase airway damage and vascular leakage. This positive trend toward enhanced bronchovascular permeability in DAC canine peripheral airways is consistent with the hypothesis that furosemide inhibits HIAO in part by enhancing microvascular leakage and thus counterbalancing the evaporative water loss that occurs during hyperpnea.

KW - asthma

KW - bronchovascular permeability

KW - goblet cells

KW - hyperpnea-induced bronchoconstriction

KW - mast cells

UR - http://www.scopus.com/inward/record.url?scp=0030468267&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030468267&partnerID=8YFLogxK

U2 - 10.1152/jappl.1996.81.6.2461

DO - 10.1152/jappl.1996.81.6.2461

M3 - Article

VL - 81

SP - 2461

EP - 2467

JO - Journal of Applied Physiology Respiratory Environmental and Exercise Physiology

JF - Journal of Applied Physiology Respiratory Environmental and Exercise Physiology

SN - 8750-7587

IS - 6

ER -