Abstract
Summary
The intrapleural injection of 500 μg of carrageenin produces an acute inflammatory reaction in the rat in which it is possible to recover quantitatively the inflammatory cells that are mobilized and the exudate. The time courses of exudate formation and neutrophil mobilization strongly suggest that these phenomena are related. Both curves are sigmoid, and increase sharply between the first and third hours. Aspirin at 90 mg/kg, p.o., produced 83% inhibition of exudate formation at three hours but by the seventh hour the inhibition was only 31%. Neutrophil mobilization was only slightly inhibited by aspirin at three hours. However, the neutrophil mobilization which occurred between the third and seventh hours was completely blocked by aspirin. Monocyte mobilization started two hours after injection of the carrageenin and continued at a fixed rate through the seventh hour. There was no mobilization of monocytes in the aspirin-treated animals for the first five hours. Thereafter the rate of mobilization of these cells was similar in control and aspirin-treated animals.
Three lines of evidence suggest that the single period of edema formation produced by the intrapleural injection of carrageenin in the first 5 hr is analogous to the second phase of the biphasic rat hindlimb reaction to this irritant. The major portion of these edemas is formed 1–3 hr after injection of carrageenin. Temporally associated with the development of both edemas is the mobilization of large numbers of neutrophils and the appearance of these cells free in the inflamed tissue. Finally, both edemas are strongly inhibited by relatively low doses of aspirin and both are insensitive to the antihistaminic triprolidine and the antiserotonin agent cyproheptadine.
The authors wish to thank Dr. Robert A. Maxwell, Dr. Donald H. Namm, and Dr. Helen L. White for their advice and constructive criticism in the preparation of this manuscript.
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