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Tenoxicam and indomethacin were studied with regard to their effects to modulate mediator release (histamine, prostaglandin E2 (PGE2) mono-hydroxyeicosatetraenoic acids, leukotrienes) from various cells. For histamine release human lymphocytes, monocytes, and basophils were analyzed with either anti-IgE or the calcium ionophore A 23187. Rat mast cells were stimulated with the calcium ionophore A 23187. With tenoxicam significant inhibition of histamine release was obtained as compared to the effects of indomethacin. Enhancement of histamine release at defined concentrations was more often observed with indomethacin than with tenoxicam. At high concentrations of indomethacin the formation of the radiolabelled phospholipids and 5S-hydroxy-6-trans-8,11,14-cis-eicosatetraenoic acid (14C-arachidonic acid metabolites) from stimulated human polymorphonuclear neutrophilic leukocytes was inhibited. With regard to endogenous leukotriene and PGE2 release tenoxicam inhibited leukotrienes B4 and C4 and PGE2 release. Tenoxicam appeared to be more active than indomethacin.
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November 1987,
The American review of respiratory disease,
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April 1984,
Japanese journal of pharmacology,
W König, and
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April 1999,
Anesthesia and analgesia,
W König, and
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January 2004,
The Kaohsiung journal of medical sciences,
W König, and
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March 1992,
Archives of ophthalmology (Chicago, Ill. : 1960),
W König, and
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September 1984,
The British journal of ophthalmology,
W König, and
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May 1987,
Arzneimittel-Forschung,
W König, and
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December 1985,
Zentralblatt fur Bakteriologie, Mikrobiologie und Hygiene. 1. Abt. Originale B, Hygiene,
W König, and
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June 1988,
Agents and actions,
W König, and
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M Stüning
September 1987,
Life sciences,
