Catalase, peroxidase and superoxide dismutase were found to inhibit significantly carrageenin edema and the primary phase of adjuvant arthritis in rats after i.v. injection. Heat-inactivated enzymes were as effective as the native enzymes. None of 10 scavengers of oxygen radicals inhibited the adjuvant arthritis at any time. Accordingly, no evidence for a participation of oxygen radicals in the secondary arthritis phase could be found, whereas a role of oxygen radicals in the primary arthritis phase and in carrageenin edema cannot be ruled out.

Among different carrageenins, kappa-carrageenans were found to be thrombogenic, whereas lambda-carrageenins were inactive in this respect, although the latter substances exerted a stronger edemogenic activity. Kappa-carrageenin (Sigma) was the most potent thrombogen. As the consequence of thrombosis tail infarction became visible some minutes after i.v. administration, but it was delayed for about 3 hours after the i.p. route and for about 6 hours after subplantar injection. Infarction frequency as well as extent of infarction was inhibited by heparin, cyproheptadine, phentolamine and dibenamine. Other substances like aspirin and dipyridamole showed no or only weak effects. Advantages of the carrageenin-induced thrombosis model in rats and mice are: (i) simple induction in small laboratory animals, (ii) easy observation and quantification all the time without killing the animals, and (iii) possible external testing of antithrombotic agents by applying substances on the tail.

The antiinflammatory action of dexamethasone in both phases of rat adjuvant arthritis was significantly reduced by injection of the RNA synthesis inhibitor actinomycin D into the inflamed paw. This effect is apparently caused by inhibition of RNA/protein synthesis and not by actinomycin D irritant activity. Thus, the present data support the view of indirect glucocorticoid activity via gene expression also in subacute and chronic adjuvant arthritis. The dexamethasone-induced antiinflammatory protein seems to be synthetized at the site of inflammation.

During 6-sulphanilamidoindazole (6-SAI) arthritis a significant increase of serum levels of the protease inhibitor alpha 2 macroglobulin (= alpha 2 acute phase globulin) and of Darcy's glycoprotein was found, whereas the content of female specific protein and of sulfhydryl groups was proved to be significantly decreased. Intravenous administration of 5 mg/kg soybean trypsin inhibitor, twice daily for 4 days, was without any inhibitory effect on paw swelling in 6-SAI arthritis but it caused increased serum levels of alpha 2 macroglobulin and Darcy's glycoprotein. Thus, spontaneous remission of 6-SAI arthritis occurring, despite continued administration of 6-SAI, seems hardly likely to be caused by acute-phase reactants, e.g. via protease inhibition. Evidence is presented which shows that spontaneous remission of 6-SAI arthritis could be due to local processes.