Abstract
Recently various component phenomena of the inflammatory reaction such as hyperemia, increasing vascular permeability, neutrophil infiltration, hemorrhage, and fibrin formation have been become measurable quantitatively using radio-labeled tracers, and have become induciable individually using purified or synthetic chemical mediators specific for each reaction. Using the techniques it has become increasingly apparent that the component of inflammation, which were considered as distinct processes, have stronger influences among them than previously appreciated. (1) It was previously noticed that when prostaglandins (E, I) were simultaneously injected with permeability inducing agents such as histamine and bradykinin, the plasma leakage caused by the agents was strongly augmented. In the recent works there have been shown many evidences that this effect of prostaglandins is attributable to hyperemia caused by them, and that this phenomenon actually occurs in several acute inflammation models. The mechanisms of the augmentation are regared as sum of effects such as increase of velocity of plasma efflux at each leaking site, increase of number of post capillary venules leaked, and increase of duration of the leakage at each site. The latter two were revealed by vital microscopic and electron microscopic observations of the microvasculature in hamster cheek pouch. (2) It has been indicated that neutrophil may be involved directly in the vascular permeability changes. For example, long lasting permeability reaction induced by chemotactic factors such as C5a, C5a des Arg, N-formyl-methionyl-leucyl-phenylalanine, and leukotreine B4 is significantly reduced in neutrophenic animals, and the time course of the permeability change appeared to parallel that of neutrophil efflux. Furthermore, in acute inflammation models, participation of this type permeability reaction was observed. It is claimed that this type permeability change is hyperemiadependent or at least strongly augmented by it.
That these recent observations must make strong influences on the research for chemical mediation of inflammatory reaction, is finally discussed.
