Surfactant dysfunction makes lungs vulnerable to repetitive collapse and reexpansion

Varsha Surendranath Taskar, Joseph John, Eva Evander, Bengt Robertson, Björn Jonson

Research output: Contribution to journalArticle

161 Citations (Scopus)

Abstract

Reexpansion of collapsed lung creates intrapulmonary shear forces. In an earlier study we showed that application of a negative end-expiratory airway pressure (NEEP) to normal rabbit lungs in vivo produced tidal collapse and reexpansion with transient changes in compliance and gas exchange but no histologic damage. In the present study we examined NEEP in a model of surfactant perturbation produced by an inhaled aerosol of 2% and 5% dioctyl sodium sulfosuccinate (DOSS). DOSS increased alveolocapillary permeability without affecting compliance or oxygenation. Repeated collapse and reexpansion (RECOREX), caused by NEEP for 3 h was compared with ventilation with positive-end expiratory pressure (PEEP). Groups ventilated with PEEP maintained normal lung mechanics and morphology even if pretreated with DOSS, NEEP disturbed lung mechanics and gas exchange with persistent dose-related histologic damage in animals pretreated with DOSS. Lungs subjected to NEEP without DOSS had normal morphology. We conclude that perturbation of the surfactant system makes lungs vulnerable to injury by RECOREX. The combination of DOSS and NEEP might lead to leakage of plasma proteins into alveoli, causing inactivation of surfactants and increased shear forces with resulting lung damage. Similar mechanisms may accelerate lung damage in the respiratory distress syndrome.

Original languageEnglish (US)
Pages (from-to)313-320
Number of pages8
JournalAmerican Journal of Respiratory and Critical Care Medicine
Volume155
Issue number1
DOIs
StatePublished - Jan 1 1997
Externally publishedYes

Fingerprint

Dioctyl Sulfosuccinic Acid
Lung
Pressure
Surface-Active Agents
Positive-Pressure Respiration
Mechanics
Compliance
Gases
Surfactant Dysfunction
Aerosols
Ventilation
Blood Proteins
Permeability
Rabbits
Wounds and Injuries

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine

Cite this

Surfactant dysfunction makes lungs vulnerable to repetitive collapse and reexpansion. / Taskar, Varsha Surendranath; John, Joseph; Evander, Eva; Robertson, Bengt; Jonson, Björn.

In: American Journal of Respiratory and Critical Care Medicine, Vol. 155, No. 1, 01.01.1997, p. 313-320.

Research output: Contribution to journalArticle

Taskar, Varsha Surendranath ; John, Joseph ; Evander, Eva ; Robertson, Bengt ; Jonson, Björn. / Surfactant dysfunction makes lungs vulnerable to repetitive collapse and reexpansion. In: American Journal of Respiratory and Critical Care Medicine. 1997 ; Vol. 155, No. 1. pp. 313-320.
@article{58bffb39e00845dc933657f6f40a6891,
title = "Surfactant dysfunction makes lungs vulnerable to repetitive collapse and reexpansion",
abstract = "Reexpansion of collapsed lung creates intrapulmonary shear forces. In an earlier study we showed that application of a negative end-expiratory airway pressure (NEEP) to normal rabbit lungs in vivo produced tidal collapse and reexpansion with transient changes in compliance and gas exchange but no histologic damage. In the present study we examined NEEP in a model of surfactant perturbation produced by an inhaled aerosol of 2{\%} and 5{\%} dioctyl sodium sulfosuccinate (DOSS). DOSS increased alveolocapillary permeability without affecting compliance or oxygenation. Repeated collapse and reexpansion (RECOREX), caused by NEEP for 3 h was compared with ventilation with positive-end expiratory pressure (PEEP). Groups ventilated with PEEP maintained normal lung mechanics and morphology even if pretreated with DOSS, NEEP disturbed lung mechanics and gas exchange with persistent dose-related histologic damage in animals pretreated with DOSS. Lungs subjected to NEEP without DOSS had normal morphology. We conclude that perturbation of the surfactant system makes lungs vulnerable to injury by RECOREX. The combination of DOSS and NEEP might lead to leakage of plasma proteins into alveoli, causing inactivation of surfactants and increased shear forces with resulting lung damage. Similar mechanisms may accelerate lung damage in the respiratory distress syndrome.",
author = "Taskar, {Varsha Surendranath} and Joseph John and Eva Evander and Bengt Robertson and Bj{\"o}rn Jonson",
year = "1997",
month = "1",
day = "1",
doi = "10.1164/ajrccm.155.1.9001330",
language = "English (US)",
volume = "155",
pages = "313--320",
journal = "American Journal of Respiratory and Critical Care Medicine",
issn = "1073-449X",
publisher = "American Thoracic Society",
number = "1",

}

TY - JOUR

T1 - Surfactant dysfunction makes lungs vulnerable to repetitive collapse and reexpansion

AU - Taskar, Varsha Surendranath

AU - John, Joseph

AU - Evander, Eva

AU - Robertson, Bengt

AU - Jonson, Björn

PY - 1997/1/1

Y1 - 1997/1/1

N2 - Reexpansion of collapsed lung creates intrapulmonary shear forces. In an earlier study we showed that application of a negative end-expiratory airway pressure (NEEP) to normal rabbit lungs in vivo produced tidal collapse and reexpansion with transient changes in compliance and gas exchange but no histologic damage. In the present study we examined NEEP in a model of surfactant perturbation produced by an inhaled aerosol of 2% and 5% dioctyl sodium sulfosuccinate (DOSS). DOSS increased alveolocapillary permeability without affecting compliance or oxygenation. Repeated collapse and reexpansion (RECOREX), caused by NEEP for 3 h was compared with ventilation with positive-end expiratory pressure (PEEP). Groups ventilated with PEEP maintained normal lung mechanics and morphology even if pretreated with DOSS, NEEP disturbed lung mechanics and gas exchange with persistent dose-related histologic damage in animals pretreated with DOSS. Lungs subjected to NEEP without DOSS had normal morphology. We conclude that perturbation of the surfactant system makes lungs vulnerable to injury by RECOREX. The combination of DOSS and NEEP might lead to leakage of plasma proteins into alveoli, causing inactivation of surfactants and increased shear forces with resulting lung damage. Similar mechanisms may accelerate lung damage in the respiratory distress syndrome.

AB - Reexpansion of collapsed lung creates intrapulmonary shear forces. In an earlier study we showed that application of a negative end-expiratory airway pressure (NEEP) to normal rabbit lungs in vivo produced tidal collapse and reexpansion with transient changes in compliance and gas exchange but no histologic damage. In the present study we examined NEEP in a model of surfactant perturbation produced by an inhaled aerosol of 2% and 5% dioctyl sodium sulfosuccinate (DOSS). DOSS increased alveolocapillary permeability without affecting compliance or oxygenation. Repeated collapse and reexpansion (RECOREX), caused by NEEP for 3 h was compared with ventilation with positive-end expiratory pressure (PEEP). Groups ventilated with PEEP maintained normal lung mechanics and morphology even if pretreated with DOSS, NEEP disturbed lung mechanics and gas exchange with persistent dose-related histologic damage in animals pretreated with DOSS. Lungs subjected to NEEP without DOSS had normal morphology. We conclude that perturbation of the surfactant system makes lungs vulnerable to injury by RECOREX. The combination of DOSS and NEEP might lead to leakage of plasma proteins into alveoli, causing inactivation of surfactants and increased shear forces with resulting lung damage. Similar mechanisms may accelerate lung damage in the respiratory distress syndrome.

UR - http://www.scopus.com/inward/record.url?scp=0031036876&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031036876&partnerID=8YFLogxK

U2 - 10.1164/ajrccm.155.1.9001330

DO - 10.1164/ajrccm.155.1.9001330

M3 - Article

C2 - 9001330

AN - SCOPUS:0031036876

VL - 155

SP - 313

EP - 320

JO - American Journal of Respiratory and Critical Care Medicine

JF - American Journal of Respiratory and Critical Care Medicine

SN - 1073-449X

IS - 1

ER -