Direct Effect of Corticotropin (ACTH) on Capillary Permeability in Inflammation

¹ From the Agnes Barr Chase Foundation for Cancer Research, Temple University School of Medicine, Philadelphia, Pennsylvania

A series of experiments are described which indicates that corticotropin directly suppresses the increased capillary permeability at the site of inflammation without necessitating the mediation of the adrenals. The increased capillary permeability in an acutely inflamed area is referable to the liberation by the injured cells of two chemical factors: leukotaxine, repressed by cortisone, primarily liberated in the incipient alkaline stage; and exudin, repressed by corticotropin, chiefly released at a later or acid stage of the inflammatory reaction. The direct daily injections of corticotropin into an inflamed area at an acid ph in a dog, yields an exudate which progressively becomes incapable of increasing capillary permeability in the skin of a rabbit, as gauged by the local accumulation of trypan blue from the circulation. A similar picture is encountered when exudin is extracted from such samples of acid exudate. The capacity of exudin to induce increased capillary permeability is also gradually diminished following direct daily injections of corticotropin into the area of pleural inflammation. In adrenalectomized rats, exudin combined with corticotropin is likewise unable to induce an increased capillary permeability, in contrast to the normal accumulation of the dye in a skin area treated only with exudin. Furthermore, the direct effect of ACTH on capillary permeability in inflammation is not referable to an impurity in commercial ACTH, for similar suppressing effects are obtained with the use of the hormone in pure form, namely alpha-corticotropin.