VASCULAR-RESPONSES DURING ACUTE NEUTROPHILIC INFLAMMATION THEIR RELATIONSHIP TO INVIVO NEUTROPHIL EMIGRATION

Abstract

Hyperemia, an increase in vascular permeability, and the emigration of leukocytes are the basic manifestations of the acute inflammatory reaction. Many previous studies have employed phagocytosable material to induce inflammation and neutrophil infiltration. Neutrophil infiltration into rabbit skin was here induced by injecting the soluble chemotactic stimuli, zymosan-activated plasma, C5adesArg, N-formyl-methionyl-leucyl-phenylalanine and factors released by Escherichia coli. During the evolution of the response, 51Cr-labeled leukocytes were used to quantitate neutrophil influx, 125I-labeled albumin was used to quantitate permeability and 86Rb was used to quantitate blood flow. Simultaneous measurements showed a close correlation in time between the degree and peak rate of neutrophil influx and the degree of hyperpermeability and hyperemia. Dose-response experiments performed with 2-90% (vol/vol) zymosan-activated plasma showed a direct correlation between the rate of neutrophil influx and the degree of vascular permeability and blood flow. No vascular responses were induced after injection of these chemotactic stimuli into rabbits made neutropenic with nitrogen mustard treatment. The vascular responses associated with neutrophil infiltration were inhibited by indomethacin or aspirin. Vascular hyperpermeability and hypermia accompanying neutrophilic inflammatory reactions may be induced by neutrophils during their migration across the microvascular walls. Prostaglandins may in part mediate these responses. Phagocytosis by the neutrophils is not required to induce these vascular changes.