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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1997-10-9
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pubmed:abstractText |
Acute lung injury (ALI) is characterized by pulmonary hypertension. Although the pathophysiology of ALI is complex, cytokine production, especially tumor necrosis factor-alpha (TNF-alpha), is known to mediate histologic lung injury. Pentoxifylline (PTX) is known to inhibit the expression of many cytokines, including TNF-alpha. The purpose of this study was to determine the effect of PTX treatment on endotoxin-induced impairment of endothelium-dependent mechanisms of pulmonary vasorelaxation. Mechanisms of endothelium-dependent relaxation were studied with the muscarinic receptor agonist, acetylcholine (ACh), and the receptor-independent calcium ionophore, A23187. Endothelium-independent pulmonary vasorelaxation was examined by direct stimulation of smooth muscle guanylate cyclase with the nitric oxide donor, sodium nitroprusside (SNP). Five rats received PTX (50 mg/kg) and endotoxin (20 mg/kg), endotoxin alone, or saline ip. After 6 hr, dose-response curves to ACh, A23187, and SNP were determined in isolated pulmonary artery rings preconstricted with phenylephrine (PE). PTX attenuated but did not eliminate endotoxin-induced impairment of endothelium-dependent and -independent pulmonary vasorelaxation. These data suggest that PTX may offer a therapeutic modality for the treatment of pulmonary hypertension in ALI.
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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/Endotoxins,
http://linkedlifedata.com/resource/pubmed/chemical/Nitroprusside,
http://linkedlifedata.com/resource/pubmed/chemical/Pentoxifylline,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphodiesterase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0022-4804
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 1997 Academic Press.
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pubmed:issnType |
Print
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pubmed:volume |
71
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
150-4
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:9299283-Animals,
pubmed-meshheading:9299283-Endothelium, Vascular,
pubmed-meshheading:9299283-Endotoxins,
pubmed-meshheading:9299283-Male,
pubmed-meshheading:9299283-Nitroprusside,
pubmed-meshheading:9299283-Pentoxifylline,
pubmed-meshheading:9299283-Phosphodiesterase Inhibitors,
pubmed-meshheading:9299283-Pulmonary Artery,
pubmed-meshheading:9299283-Rats,
pubmed-meshheading:9299283-Rats, Sprague-Dawley,
pubmed-meshheading:9299283-Respiratory Distress Syndrome, Adult,
pubmed-meshheading:9299283-Tumor Necrosis Factor-alpha,
pubmed-meshheading:9299283-Vasodilation
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pubmed:year |
1997
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pubmed:articleTitle |
Pentoxifylline treatment attenuates pulmonary vasomotor dysfunction in acute lung injury.
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pubmed:affiliation |
Department of Surgery, University of Colorado, Denver, Colorado, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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