Abstract
Group B streptococci (GBS) cause fatal sepsis in newborns. Strong activation of thromboxane synthesis is assumed to correlate with severe pulmonary hypertension. In this study we compared the impact of indomethacin versus parecoxib on hemodynamics and outcome and investigated the pharmacological effects on thromboxane synthesis and EP-3 receptor gene expression. Whereas both parecoxib and indometacin reduced expression of thromboxane synthase and EP-3 receptor in infected lung tissue, parecoxib did not suppress urine levels of thromboxane like indometacin. We presume that COX-2 inhibition in GBS sepsis is associated with enhanced thrombogenicity.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Animals, Newborn
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Cyclooxygenase 2 Inhibitors / pharmacology*
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Dinoprostone / urine
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Epoprostenol / metabolism
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Epoprostenol / urine
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Gene Expression Regulation / drug effects
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Hemodynamics / drug effects
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Indomethacin / pharmacology
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Inflammation / metabolism
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Inflammation / pathology
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Inflammation / urine
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Isoxazoles / pharmacology*
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Lung / drug effects
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Lung / pathology
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Platelet Count
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Receptors, Prostaglandin E / metabolism
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Sepsis / metabolism*
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Sepsis / pathology
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Sepsis / physiopathology
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Sepsis / urine
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Streptococcal Infections / metabolism*
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Streptococcal Infections / microbiology
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Streptococcal Infections / pathology
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Streptococcal Infections / urine
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Streptococcus agalactiae*
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Swine
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Thromboxanes / biosynthesis*
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Thromboxanes / metabolism
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Thromboxanes / urine
Substances
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Cyclooxygenase 2 Inhibitors
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Isoxazoles
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Receptors, Prostaglandin E
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Thromboxanes
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parecoxib
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Epoprostenol
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Dinoprostone
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Indomethacin