Abstract
IT has been suggested recently that lipid substances may play a part in the mediation of inflammatory events1,2. One of these lipids, slow reacting substance C (SRS-C), probably an unsaturated fatty acid or derivative, is released when egg yolk lecithin or guinea-pig lung is challenged by venoms containing phospholipase A3. Another liposoluble spasmogen which is released by guinea-pig lung during in vitro anaphylaxis is called slow reacting substance A (SRS-A)2. SRS-A increases the resistance of lungs to inflation and this activity is blocked by non-steroidal anti-inflammatory agents4. The structure of SRS-A has not yet been elucidated, but the pharmacological activity on isolated human tracheal muscle of at least one identified lipid derivative, prostaglandin F2a (PGF2a), was blocked by the same agents1. Here we present evidence of the pharmacological activity of SRS-C and its blockade by non-steroidal anti-inflammatory agents. We suggest that in some preparations SRS-C may share the same receptor sites as the polypeptide kinins, or block the route from the specific receptors for the agonists.
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VARGAFTIG, B., DE MIRANDA, E. & LACOUME, B. Inhibition by Non-steroidal Anti-inflammatory Agents of in vivo Effects of “Slow Reacting Substance C”. Nature 222, 883–885 (1969). https://doi.org/10.1038/222883a0
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DOI: https://doi.org/10.1038/222883a0
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