Involvement of arachidonic acid metabolites in increases in vascular permeability in experimental dental pulpal inflammation in the rat.
Pulp was experimentally inflamed by applying bacterial lipopolysaccharide (LPS). Changes in arachidonic acid (AA) metabolites were determined by measuring the conversion of exogenously added AA in pulp homogenates. The inflamed pulp produced 12-hydroxy-eicosatetraenoic acid (12-HETE), 6-keto-prostaglandin (PG) F1 alpha greater than PGE2, thromboxane B2 and 11-HETE, which was further identified with high-performance liquid chromatography. The LPS treatment caused a 2.0-fold increase in 12-HETE production at 1 h, a 3.8-fold increase in 6-keto-PGF1 alpha production at 12 h and increases in PGE2 and 11-HETE production of 8.8- and 5.5-fold, respectively, at 24 h. Vascular permeability in the inflamed pulp was measured by quantifying the amount of an extravasated dye; it increased markedly from 6 h and reached a peak at 12 h after the LPS application. When indomethacin (0.3-30 mg/kg, s.c.) was given before LPS, both the production of 6-keto-PGF1 alpha and PGE2 and the increase in vascular permeability were inhibited dose dependently. Exogenously applied PGE2 and PGI2 methyl ester reduced the inhibition of the increase in vascular permeability caused by indomethacin. Thus PGE2 and PGI2 may be involved in increases in vascular permeability in pulpal inflammation.
Okiji
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T
Department of Endodontics, Faculty of Dentistry, Tokyo Medical and Dental University, Japan.
Morita
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Sunada
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Murota
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S
D019377:12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis* / Q000502:physiology; D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism*; D002199:Capillary Permeability / Q000187:drug effects*; D002851:Chromatography, High Pressure Liquid; D003782:Dental Pulp / Q000098:blood supply; D015232:Dinoprostone / Q000096:biosynthesis / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D006893:Hydroxyeicosatetraenoic Acids / Q000096:biosynthesis* / Q000502:physiology; D007213:Indomethacin / Q000494:pharmacology; D008070:Lipopolysaccharides; D008297:Male; D011671:Pulpitis / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology; D051381:Rats; D011919:Rats, Inbred Strains; D013929:Thromboxane B2 / Q000096:biosynthesis* / Q000502:physiology
D001095:Arachidonic Acids; D006893:Hydroxyeicosatetraenoic Acids; D008070:Lipopolysaccharides; D016718:Arachidonic Acid; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D019377:12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; C027356:11-hydroxy-5,8,12,14-eicosatetraenoic acid; D015232:Dinoprostone; D007213:Indomethacin