An inflammatory reaction forms a prominent part of the biochemical and physiological processes involved in the acute rejection of tissue and organ allografts. Significant increase in the size of the transplanted organ with edema and cellular infiltration is a constant feature of acute rejection. In most instances, this process is reversible through the administration of large amounts of corticosteroids. It is probable that a significant portion of the effect of corticosteroids on the reversal of acute allograft rejection is anti-inflammatory.
Unpublished as well as published evidence has been obtained in recent years by us and our associates,1-10 suggesting an involvement of accelerated intracellular histamine formation and release in acute allograft rejection. An increase in intracellular histamine formation from histidine decarboxylase enzyme activity during allograft rejection has been found both at the site of allograft rejection and in distant immunologically involved lymphoid tissue.7,8 Inhibitors of the histamine-forming enzyme have