RESUMO
1. Injection of carrageenin into the liver of rats provoked a focal necrotic-hemorrhagic lesion that evolved through acute inflammation, accumulation of macrophages and fibroblasts and the formation of a relatively large amount of fibrous tissue that underwent resorption. The entire lesion disappeared within15-18 days of the beginning of incolulation. 2. Ultrastructural analysis revealed that carrageenin granules were taken up by macrophages, fibroblasts and myofibroblasts and that signs of formation and degradation of collagen were constant features, the former predominating early and the latter being evident to ward the second half of the evolution of the lesion. 3. The presence of fibronection was prominent during the first days and Type I and type III collagens were present in the extracellular matrix soon after induction of the carrageenin lesion. Both collagen isotypes subsequently underwent progressive and simultaneous resorption. 4. The rapid formation and degradation of both collagen isotypes during the evolution of carrageenin granuloma indicates that collagen stability is not fundamentally dependent on genetic isotype