Evidence for lipoxygenase pathway involvement in allergic tracheal contraction
| Autor: | N.A.M. Paterson, J.F. Burka |
|---|---|
| Rok vydání: | 1980 |
| Předmět: |
Male
Prostaglandins E Synthetic Contraction (grammar) medicine.medical_treatment Guinea Pigs Indomethacin Lipoxygenase Arachidonic Acids Constriction Pathologic Pharmacology Phenidone In Vitro Techniques Biochemistry chemistry.chemical_compound Endocrinology medicine Hypersensitivity Animals Tracheal Diseases biology Aspirin Metabolism respiratory system Asthma chemistry Meclofenamate Sodium biology.protein lipids (amino acids peptides and proteins) Arachidonic acid SRS-A Histamine Prostaglandin E |
| Zdroj: | Prostaglandins. 19(4) |
| ISSN: | 0090-6980 |
| Popis: | Challenge of actively sensitized guinea-pig trachea in vitro led to a contraction which was enhanced by the cyclo-oxygenase inhibitors, indomethacin and sodium meclofenamate. Cyclo-oxygenase inhibitors eliminated the release of PGE-like material induced by arachidonic acid (AA), histamine, and antigen challenge. AA (10 microgram./ml.) and PGE2 (100 ng./ml.) usually relaxed the trachea, whereas in the presence of cyclo-oxygenase inhibitors a contraction occurred. Phenidone and ETYA, which also blocked the lipoxygenase pathway of AA metabolism inhibited the enhancement of allergic tracheal contraction induced by cyclo-oxygenase inhibitors, decreased the time that the trachea remained contracted, and also eliminated the contraction induced by AA and PGE2. Thus, cyclo-oxygenase inhibitors may enhance allergic tracheal contraction by diverting AA metabolism into the lipoxygenase pathway and product of the latter pathway, possibly SRS-A, may be responsible for the enhancement and for the prolonged phase of allergic tracheal contraction. An analogous mechanism may account for aspirin-induced asthma in man. |
| Databáze: | OpenAIRE |
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