Leukotrienes and Slow Reacting Substance of Anaphylaxis (SRS‐A)

In 1938 Feldberg & Kellaway demonstrated that perfusates from dog and monkey lungs, treated with cobra venom, induced sustained contractions with slow onset on isolated guinea pig jejunum (19). Kellaway & Trethewie (26) named the active principle "slow reacting substance" (SRS) and showed that SRS was released by immunological challenge of sensitized guinea pig lungs. The bioassay for SRS was subsequently refined by use of a histamine antagonist (mepyramine) in the organ bath (14). The term "slow reacting substance of anaphyiaxis" (SRS-A) was introduced for immunologically released SRS and it was shown that perfused segments of human lung from asthmatic patients produced SRS-A after treatment with birch or timothy pollen. Furthermore, addition of allergens to bronchial rings from these patients resulted in a prolonged contraction of the bronchial muscle and release of SRS-A (14). This and other evidence have suggested that SRS-A is an important mediator of symptoms in asthma and other immediate hypersensitivity reactions (reviewed in 2 and 32). The proposed pathophysiological importance of SRS-A stimulated research on the structure of this principle. With use of impure preparations and modifiers of functional groups it was suggested that SRS is a carboxylic acid with hydroxyl group(s) and one or more double bonds (47). Similar conclusions were obtained by others who also

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