Abstract
An exudate at an alkaline pH causes a local increase in capillary permeability. This is suppressed by either adrenal cortex or by cortisone. An exudate at an acid pH induces a marked increase in local capillary permeability. Neither adrenal cortex extract nor cortisone is capable of inhibiting this effect. The increase in capillary permeability caused by an inflammatory exudate with an acid reaction is not referable to the rise in the local H- ion concn. The effect occurs concomitantly with the development of an acid pH in the inflamed area. The increase in capillary permeability induced by an exudate at an acid pH is due to a factor which seems to be neither leukotaxine nor histamine. This additional factor seems to supplement leukotaxine, the latter recovered mainly from alkaline exudates at the beginning of the acute inflammatory reaction, when the reaction progresses to an acid stage. The term exudin is tentatively proposed for this factor which offers further understanding of the mechanism of increased capillary permeability in inflammation. The relationship of exudin to physiol. homeostasis is discussed.