Abstract
These results support the hypothesis that the brain vasculature is the site of PGE2 production responsible for LPS-induced fever. LPS seems to increase the PGE2 level in the entire brain via the induction of COX-2. Fever may be mediated by PGE2 which is produced in the blood vessels in the preoptic area or which is produced in other parts of the brain and transported to the preoptic area through the ventricular system.
MeSH terms
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Animals
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Brain / blood supply
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Brain / enzymology*
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Cyclooxygenase 2
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Cyclooxygenase 2 Inhibitors
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Cyclooxygenase Inhibitors / pharmacology
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Dinoprostone / metabolism
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Fever / physiopathology
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Gene Expression Regulation
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Isoenzymes / physiology*
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Lipopolysaccharides / pharmacology
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Neurons / enzymology
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Nitrobenzenes / pharmacology
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Prostaglandin-Endoperoxide Synthases / physiology*
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RNA, Messenger / genetics
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Rats
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Sulfonamides / pharmacology
Substances
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Cyclooxygenase 2 Inhibitors
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Cyclooxygenase Inhibitors
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Isoenzymes
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Lipopolysaccharides
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Nitrobenzenes
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RNA, Messenger
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Sulfonamides
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N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide
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Cyclooxygenase 2
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Prostaglandin-Endoperoxide Synthases
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Dinoprostone