Dibutyryl cAMP, aminophylline, and β-adrenergic agonists protect against pulmonary edema caused by phosgene

T. P. Kennedy, J. R. Michael, J. R. Hoidal, D. Hasty, A. M. Sciuto, C. Hopkins, R. Lazar, G. K. Bysani, Elizabeth Tolley, G. H. Gurtner

Research output: Contribution to journalArticle

59 Citations (Scopus)

Abstract

Phosgene is a toxic oxidant gas that causes the adult respiratory distress syndrome in exposed workers. Phosgene exposure markedly increased lung weight gain in buffer-perfused isolated rabbit lungs (31 ± 5 g over 60 min after phosgene vs. 7.7 ± 1.2 in control lungs, P < 0.01) and markedly increased the lung leak index for 125I-albumin (0.28 ± 0.03 after phosgene vs. 0.02 ± 0.01 in control lungs, P < 0.01). Pretreatment with dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP), aminophylline, or terbutaline plus isoproterenol prevented the increase in lung weight caused by phosgene (31 ± 5 g phosgene, 11.7 ± 2.8 DBcAMP, 7.5 ± 2.5 aminophylline, 6.1 ± 1 terbutaline and isoproterenol, 6.1 ± 1.2 control + aminophylline, and 7.7 ± 1.2 control; all treatments were P < 0.01 vs. the untreated phosgene group and not significantly different from control lungs). Pretreatment with aminophylline prevented the increase in lung leak index for 125I-albumin (0.28 ± 0.03 after phosgene vs. 0.06 ± 0.02 in aminophylline-treated lungs, P < 0.01). Posttreatment with aminophylline and terbutaline also prevented the increase in lung weight caused by phosgene. These results indicate that phosgene dramatically increased the movement of fluid and protein across the pulmonary vasculature and that treatment with DBcAMP, aminophylline, terbutaline, or isoproterenol markedly reduces the pulmonary edema caused by phosgene.

Original languageEnglish (US)
Pages (from-to)2542-2552
Number of pages11
JournalJournal of applied physiology
Volume67
Issue number6
StatePublished - Dec 1 1989

Fingerprint

Phosgene
Aminophylline
Adrenergic Agonists
Pulmonary Edema
Lung
Terbutaline
Bucladesine
Isoproterenol
Albumins
Weights and Measures
Poisons
Adult Respiratory Distress Syndrome
Oxidants
Weight Gain

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

Kennedy, T. P., Michael, J. R., Hoidal, J. R., Hasty, D., Sciuto, A. M., Hopkins, C., ... Gurtner, G. H. (1989). Dibutyryl cAMP, aminophylline, and β-adrenergic agonists protect against pulmonary edema caused by phosgene. Journal of applied physiology, 67(6), 2542-2552.

Dibutyryl cAMP, aminophylline, and β-adrenergic agonists protect against pulmonary edema caused by phosgene. / Kennedy, T. P.; Michael, J. R.; Hoidal, J. R.; Hasty, D.; Sciuto, A. M.; Hopkins, C.; Lazar, R.; Bysani, G. K.; Tolley, Elizabeth; Gurtner, G. H.

In: Journal of applied physiology, Vol. 67, No. 6, 01.12.1989, p. 2542-2552.

Research output: Contribution to journalArticle

Kennedy, TP, Michael, JR, Hoidal, JR, Hasty, D, Sciuto, AM, Hopkins, C, Lazar, R, Bysani, GK, Tolley, E & Gurtner, GH 1989, 'Dibutyryl cAMP, aminophylline, and β-adrenergic agonists protect against pulmonary edema caused by phosgene', Journal of applied physiology, vol. 67, no. 6, pp. 2542-2552.
Kennedy TP, Michael JR, Hoidal JR, Hasty D, Sciuto AM, Hopkins C et al. Dibutyryl cAMP, aminophylline, and β-adrenergic agonists protect against pulmonary edema caused by phosgene. Journal of applied physiology. 1989 Dec 1;67(6):2542-2552.
Kennedy, T. P. ; Michael, J. R. ; Hoidal, J. R. ; Hasty, D. ; Sciuto, A. M. ; Hopkins, C. ; Lazar, R. ; Bysani, G. K. ; Tolley, Elizabeth ; Gurtner, G. H. / Dibutyryl cAMP, aminophylline, and β-adrenergic agonists protect against pulmonary edema caused by phosgene. In: Journal of applied physiology. 1989 ; Vol. 67, No. 6. pp. 2542-2552.
@article{c79a35d6a2d948e3b80c668aa50d2430,
title = "Dibutyryl cAMP, aminophylline, and β-adrenergic agonists protect against pulmonary edema caused by phosgene",
abstract = "Phosgene is a toxic oxidant gas that causes the adult respiratory distress syndrome in exposed workers. Phosgene exposure markedly increased lung weight gain in buffer-perfused isolated rabbit lungs (31 ± 5 g over 60 min after phosgene vs. 7.7 ± 1.2 in control lungs, P < 0.01) and markedly increased the lung leak index for 125I-albumin (0.28 ± 0.03 after phosgene vs. 0.02 ± 0.01 in control lungs, P < 0.01). Pretreatment with dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP), aminophylline, or terbutaline plus isoproterenol prevented the increase in lung weight caused by phosgene (31 ± 5 g phosgene, 11.7 ± 2.8 DBcAMP, 7.5 ± 2.5 aminophylline, 6.1 ± 1 terbutaline and isoproterenol, 6.1 ± 1.2 control + aminophylline, and 7.7 ± 1.2 control; all treatments were P < 0.01 vs. the untreated phosgene group and not significantly different from control lungs). Pretreatment with aminophylline prevented the increase in lung leak index for 125I-albumin (0.28 ± 0.03 after phosgene vs. 0.06 ± 0.02 in aminophylline-treated lungs, P < 0.01). Posttreatment with aminophylline and terbutaline also prevented the increase in lung weight caused by phosgene. These results indicate that phosgene dramatically increased the movement of fluid and protein across the pulmonary vasculature and that treatment with DBcAMP, aminophylline, terbutaline, or isoproterenol markedly reduces the pulmonary edema caused by phosgene.",
author = "Kennedy, {T. P.} and Michael, {J. R.} and Hoidal, {J. R.} and D. Hasty and Sciuto, {A. M.} and C. Hopkins and R. Lazar and Bysani, {G. K.} and Elizabeth Tolley and Gurtner, {G. H.}",
year = "1989",
month = "12",
day = "1",
language = "English (US)",
volume = "67",
pages = "2542--2552",
journal = "Journal of Applied Physiology",
issn = "8750-7587",
publisher = "American Physiological Society",
number = "6",

}

TY - JOUR

T1 - Dibutyryl cAMP, aminophylline, and β-adrenergic agonists protect against pulmonary edema caused by phosgene

AU - Kennedy, T. P.

AU - Michael, J. R.

AU - Hoidal, J. R.

AU - Hasty, D.

AU - Sciuto, A. M.

AU - Hopkins, C.

AU - Lazar, R.

AU - Bysani, G. K.

AU - Tolley, Elizabeth

AU - Gurtner, G. H.

PY - 1989/12/1

Y1 - 1989/12/1

N2 - Phosgene is a toxic oxidant gas that causes the adult respiratory distress syndrome in exposed workers. Phosgene exposure markedly increased lung weight gain in buffer-perfused isolated rabbit lungs (31 ± 5 g over 60 min after phosgene vs. 7.7 ± 1.2 in control lungs, P < 0.01) and markedly increased the lung leak index for 125I-albumin (0.28 ± 0.03 after phosgene vs. 0.02 ± 0.01 in control lungs, P < 0.01). Pretreatment with dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP), aminophylline, or terbutaline plus isoproterenol prevented the increase in lung weight caused by phosgene (31 ± 5 g phosgene, 11.7 ± 2.8 DBcAMP, 7.5 ± 2.5 aminophylline, 6.1 ± 1 terbutaline and isoproterenol, 6.1 ± 1.2 control + aminophylline, and 7.7 ± 1.2 control; all treatments were P < 0.01 vs. the untreated phosgene group and not significantly different from control lungs). Pretreatment with aminophylline prevented the increase in lung leak index for 125I-albumin (0.28 ± 0.03 after phosgene vs. 0.06 ± 0.02 in aminophylline-treated lungs, P < 0.01). Posttreatment with aminophylline and terbutaline also prevented the increase in lung weight caused by phosgene. These results indicate that phosgene dramatically increased the movement of fluid and protein across the pulmonary vasculature and that treatment with DBcAMP, aminophylline, terbutaline, or isoproterenol markedly reduces the pulmonary edema caused by phosgene.

AB - Phosgene is a toxic oxidant gas that causes the adult respiratory distress syndrome in exposed workers. Phosgene exposure markedly increased lung weight gain in buffer-perfused isolated rabbit lungs (31 ± 5 g over 60 min after phosgene vs. 7.7 ± 1.2 in control lungs, P < 0.01) and markedly increased the lung leak index for 125I-albumin (0.28 ± 0.03 after phosgene vs. 0.02 ± 0.01 in control lungs, P < 0.01). Pretreatment with dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP), aminophylline, or terbutaline plus isoproterenol prevented the increase in lung weight caused by phosgene (31 ± 5 g phosgene, 11.7 ± 2.8 DBcAMP, 7.5 ± 2.5 aminophylline, 6.1 ± 1 terbutaline and isoproterenol, 6.1 ± 1.2 control + aminophylline, and 7.7 ± 1.2 control; all treatments were P < 0.01 vs. the untreated phosgene group and not significantly different from control lungs). Pretreatment with aminophylline prevented the increase in lung leak index for 125I-albumin (0.28 ± 0.03 after phosgene vs. 0.06 ± 0.02 in aminophylline-treated lungs, P < 0.01). Posttreatment with aminophylline and terbutaline also prevented the increase in lung weight caused by phosgene. These results indicate that phosgene dramatically increased the movement of fluid and protein across the pulmonary vasculature and that treatment with DBcAMP, aminophylline, terbutaline, or isoproterenol markedly reduces the pulmonary edema caused by phosgene.

UR - http://www.scopus.com/inward/record.url?scp=0024847507&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024847507&partnerID=8YFLogxK

M3 - Article

VL - 67

SP - 2542

EP - 2552

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 8750-7587

IS - 6

ER -