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T
he two pyrazolon derivatives, phenylbutazone and sulfinpyrazone, selectively inhibit chemotactic peptide-induced effects on neutrophils. As they antagonize the induction of acute neutropenia in vivo and of cellular hyperadhesiveness, lysosomal enzyme release, hexose monophosphate shunt activity, and superoxide production in vitro, these effects occur with a specificity not shared with other prostaglandin biosynthesis inhibition by these drugs resembles the competitive type of antagonism and occurs at concentrations attainable in vivo under clinical conditions. The locomotory machinery, the direction-finding mechanisms, and the basic metabolic machinery of the cell are unaffected. These drugs interfere with specific binding of the formylpeptide to its receptor on neutrophils.
