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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
1984-7-10
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pubmed:abstractText |
alpha-Naphthyl thiourea ( ANTU ) produces pulmonary endothelial injury, pulmonary edema, and pleural effusions in rats in a dose-dependent manner. Since prostaglandins of the E series have been shown to modulate inflammatory responses in vivo and neutrophil and platelet function in vitro we investigated the effects of prostaglandin E1 (PGE1) on ANTU -induced lung injury. Systemic administration of 15-(S)-15-methyl-PGE1 (15-M-PGE1), a stable analog of PGE1, potentiated lung injury induced by ANTU in a dose- and time-dependent manner. 15-M-PGE1 (1 mg/kg, subcutaneously) administered 1 hour prior to ANTU treatment (1 mg/kg, intraperitoneally) resulted in a 164% increase (p less than 0.001) in pleural effusion formation and a 42% increase (p less than 0.02) in wet lung weight at 4 hours after ANTU administration. This was associated with increased pulmonary endothelial cell blebbing and gap formation with a decrease in the number of platelet thrombi in 15-M-PGE1-treated animals compared with controls. 15-(S)-15-methyl-prostaglandin F2 alpha, was less effective than 15-M-PGE1 in potentiating ANTU -induced lung injury. Platelet depletion, but not neutrophil depletion, also potentiated ANTU -induced lung injury, suggesting a protective role for platelets. Platelets isolated from 15-M-PGE1-treated animals demonstrated an approximately 50% decreased aggregation response to adenosine diphosphate. 15-M-PGE1 (1 mg/kg) treatment combined with platelet depletion resulted in a 1.7-fold increase (p less than 0.01) in pleural effusions in ANTU -treated (1 mg/kg) animals compared with platelet depletion alone. These studies indicate that systemic treatment of rats with 15-M-PGE1 will potentiate ANTU -induced lung injury. This injury may be in part secondary to the ability of 15-M-PGE1 to inhibit platelet function. However, platelet depletion studies suggest that 15-M-PGE1 has additional effects, possibly on endothelial cells and/or vascular smooth muscle cells that contribute to the potentiation of ANTU -induced lung injury.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/15(S)-15-methylprostaglandin E1,
http://linkedlifedata.com/resource/pubmed/chemical/Alprostadil,
http://linkedlifedata.com/resource/pubmed/chemical/Prostaglandins E, Synthetic,
http://linkedlifedata.com/resource/pubmed/chemical/Rodenticides,
http://linkedlifedata.com/resource/pubmed/chemical/Thiourea,
http://linkedlifedata.com/resource/pubmed/chemical/alpha-naphthyl thiourea
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0023-6837
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
50
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
703-10
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:6233454-Alprostadil,
pubmed-meshheading:6233454-Animals,
pubmed-meshheading:6233454-Blood Platelets,
pubmed-meshheading:6233454-Dose-Response Relationship, Drug,
pubmed-meshheading:6233454-Lung,
pubmed-meshheading:6233454-Male,
pubmed-meshheading:6233454-Microscopy, Electron,
pubmed-meshheading:6233454-Pleural Effusion,
pubmed-meshheading:6233454-Prostaglandins E, Synthetic,
pubmed-meshheading:6233454-Pulmonary Edema,
pubmed-meshheading:6233454-Rats,
pubmed-meshheading:6233454-Rats, Inbred Strains,
pubmed-meshheading:6233454-Rodenticides,
pubmed-meshheading:6233454-Specific Pathogen-Free Organisms,
pubmed-meshheading:6233454-Thiourea,
pubmed-meshheading:6233454-Time Factors
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pubmed:year |
1984
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pubmed:articleTitle |
Potentiation of alpha-naphthyl thiourea-induced lung injury by prostaglandin E1 and platelet depletion.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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