Abstract
Summary and Conclusions
Cortisone fails to obliterate the spreading reaction caused by hyaluronidase. This substance seems to inhibit at times somewhat the increased capillary permeability induced by 500 to 900 γ of hyaluronidase. An alkaline exudate or leukotaxine induces an increase in the local capillary permeability. Thus, as shown (1,2), 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 of inflammation 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 referable 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 nitrogen content of exudin is about 10%. The amino nitrogen values before and after hydrolysis suggest that one is dealing possibly with a dipeptide to which there may be a prosthetic group attached. Further studies, however, will perhaps throw more light on this point. Exudin, tested for the presence of histamine, fails to contract the strip of guinea pig intestine. When extracted for histamine by the method of Bar-soum and Gaddum, there is no evidence that exudin contains any histamine. Its behavior toward cortisone and its indiffusibility indicate that leukotaxine and histamine are dissimilar in nature to exudin.
Get full access to this article
View all access options for this article.