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Piriprost pretreatment attenuates the smoke-induced increase in 99mTcDTPA lung clearance.
- Source :
-
Experimental lung research [Exp Lung Res] 1990 Jul-Aug; Vol. 16 (4), pp. 339-53. - Publication Year :
- 1990
-
Abstract
- We studied the effects of acute smoke exposure on lung permeability, eicosanoids, and inflammatory cell activity. Thirty-five New Zealand white rabbits were anesthetized, paralyzed, and exposed to 60 tidal volume breaths of diesel fuel-polycarbonate plastic smoke or sham smoke within 10 min. At 1 h postexposure the rabbits were killed and their lungs were removed for bronchoalveolar lavage (BAL) or pathologic procedures. Smoke exposure caused decreases in technetium-labeled diethylenetriamine pentaacetate (99mTcDTPA, mol. wt. 492 Da) biological half-life (t1/2), BAL plasminogen activator, and BAL leukotriene B4 (LTB4). In addition, alveolar macrophage acid phosphatase enzyme activity increased in smoke-exposed rabbits. The leukotriene synthesis inhibitor, piriprost (U-60,257), given before smoke exposure, caused attenuation of the changes in 99mTcDTPA uptake and plasminogen activator, swelling of type I alveolar cell epithelium, a large increase in lung inflammatory cells, and decreases in BAL LTB4, prostaglandin E2 (PGE2), and TxB2 (stable metabolite of thromboxane, TxA2). We conclude that changes in alveolar-capillary barrier permeability and plasminogen activator activity occur within 1 h after exposure to smoke and may play an early role in the inflammatory process associated with smoke inhalation injury. Furthermore, piriprost attenuates the smoke-induced increase in alveolar-capillary barrier permeability and decrease in plasminogen activator activity and causes a swelling of type I alveolar epithelium. However, our data suggest that neither lung eicosanoids or the alveolar macrophage lysis process plays a major role in the smoke-induced increase in alveolar-capillary barrier permeability.
- Subjects :
- Animals
Bronchoalveolar Lavage Fluid metabolism
Bronchoalveolar Lavage Fluid pathology
Eicosanoids metabolism
Half-Life
Lung drug effects
Lung metabolism
Macrophages pathology
Organotechnetium Compounds
Pentetic Acid
Permeability
Plasminogen Activators metabolism
Rabbits
SRS-A antagonists & inhibitors
Smoke Inhalation Injury pathology
Smoke Inhalation Injury prevention & control
Technetium Tc 99m Pentetate
Epoprostenol pharmacology
Lung Injury
Smoke Inhalation Injury metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 0190-2148
- Volume :
- 16
- Issue :
- 4
- Database :
- MEDLINE
- Journal :
- Experimental lung research
- Publication Type :
- Academic Journal
- Accession number :
- 2118452
- Full Text :
- https://doi.org/10.3109/01902149009108849