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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
7 Spec No
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pubmed:dateCreated |
1989-10-12
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pubmed:abstractText |
Endogenous formation of thromboxane A2 and prostacyclin were evaluated in seven neonatates with persistent pulmonary hypertension by serial gas chromatographic mass spectrometric determination of their urinary metabolites dinor-thromboxane B2 and dinor-6-keto-prostaglandin F1 alpha, respectively. The patients were studied until their hypertension had resolved on clinical criteria. Urinary excretion of dinor-thromboxane B2 and dinor-6-keto-prostaglandin F1 alpha was increased when the persistent pulmonary hypertension was associated with group B streptococcal (n = 2) and pneumococcal (n = 1) sepsis. Based on urinary metabolite excretion, endogenous formation of thromboxane A2 and prostacyclin did not consistently differ from normal neonates in four patients with non-septic persistent pulmonary hypertension (hyaline membrane disease (n = 2), asphyxia, and meconium aspiration). These data suggest that thromboxane A2 is not a universal mediator of persistent pulmonary hypertension. It may, however, have a role in the pathophysiology of early onset group B streptococcal disease, and persistent pulmonary hypertension of other infectious aetiology. If these findings are confirmed by further studies, thromboxane synthetase inhibition or receptor antagonism may offer a potential therapeutic approach in neonates with persistent pulmonary hypertension associated with sepsis.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/2673060-2840288,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2673060-2964208,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2673060-3085564,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2673060-3100340,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2673060-3278589,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2673060-3466793,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2673060-3519915,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2673060-3520468,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2673060-3819951,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2673060-3882264,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2673060-3944270,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2673060-6342834,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2673060-6352882,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2673060-6384909,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2673060-6402752,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2673060-6546658
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1468-2044
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
64
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
949-52
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:2673060-6-Ketoprostaglandin F1 alpha,
pubmed-meshheading:2673060-Bacterial Infections,
pubmed-meshheading:2673060-Epoprostenol,
pubmed-meshheading:2673060-Female,
pubmed-meshheading:2673060-Humans,
pubmed-meshheading:2673060-Hypertension, Pulmonary,
pubmed-meshheading:2673060-Infant, Newborn,
pubmed-meshheading:2673060-Male,
pubmed-meshheading:2673060-Thromboxane A2,
pubmed-meshheading:2673060-Thromboxane B2
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pubmed:year |
1989
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pubmed:articleTitle |
Endogenous formation of prostanoids in neonates with persistent pulmonary hypertension.
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pubmed:affiliation |
Department of Paediatrics, University of Heidelberg, West Germany.
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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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