Further Studies on Mechanism of Increased Capillary Permeability in Inflammation with the Aid of Cortisone and ACTH

Abstract

Cortisone fails to obliterate the spreading reaction caused by hyaluronidge. An alkaline exudate or leukotaxine induces an increase in the local capillary permeability. Thus, as shown in 1940 and in 1942 (Menkin, Amer. Jour. Physiol. 129: 691. 1940; Proc. Soc. Exptl. Biol. and Med. 51-39. 1942). The materials are inhibited by adrenal cortical extract or by cortisone. When, however, the exudate is acid in reaction, the local increased capillary permeability is not repressed by either cortisone or by adrenal cortical extract. This is shown to be referable to another factor liberated in the later stages of an acute inflammatory reaction. This substance is concerned with the mechanism of increased capillary permeability in inflammation. This factor is termed "exudin." Consequently the initial increase in capillary permeability in the development is referable to leukotaxine. With the progress of the acute inflammation the pH of the exudate becomes acid and the mechanism of sustained increased capillary permeability is referred to exudin. The degree of acidity does not seem to be the cause of exudin formation. Exudin seems rather to be liberated about concomitantly with the development of an acid reaction in the inflamed area. The N content of exudin is about 10%. Amino N studies before and after hydrolysis support the view of a dipeptide; but this will require further confirmation. Exudin is neither leukotaxine nor histamine. Finally, the intraven. injn. of ACTH suppresses the local increase in capillary permeability referable to exudin. The possibilty of these findings in regard to a further understanding of the mechanism of ACTH in various infectious conditions is discussed.