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PubMed1981

[Suppressive effects of 5-bromuracile and 5-bromuracile-epsilon-aminocaproic acid on the humoral anti-sheep erythrocyte immune response of mice in vivo and in vitro (author's transl)].

4 x 30 mg/kg 5-bromuracile (5-BrU) - injected shortly after the antigen once per day - suppress the development of direct plaque forming cells (PFC) in the spleen of immunized mice on the 4th day of the primary reaction weakly. 5 higher doses epsilon-aminocapronic acid (ACA) were not immunosuppressive, but those of 5-BrU-ACA. The immunosuppression was of short time, 6 days later equal direct PFCs were found in the spleens of experimental and control groups. 5 x 150 mg/kg 5-BrU-ACA or ACA decreased the formation of indirect PFCs on the 10th day of immune response. In vivo 5-BrU and 5-BrU-ACA inhibited the development of non or specific stimulated spleen cells to direct PFCs only in partially cytotoxic concentrations of 5 times 10(-4) Mol.

Aminocaproates↗
PubMed1975

Inhibition by epsilon-aminocaproic acid of the activation of the first component of the complement system.

The influence of EACA on C1 in whole human serum and on C1 and C (see article) as isolated molecules was assessed hemolytically. There was selective inhibition of C1 without effect on the levels of C4, C2, C3, and C9 in whole human serum that was reversed by dialysis. EACA was found to inhibit the intrinsic activation of C1 without inhibiting the already active molecule. This was confirmed by the capacity of trypsin to uncover C1 activity in cellular intermediates formed by C1 treated with EACA that did not evolve in the absence of this extrinsic activating mechanism. Inasmuch as the trypsin-dependent recovery of C1 was incomplete, an effect on binding cannot be excluded.

Aminocaproates↗
PubMed1975

The therapeutic role of epsilon-aminocaproic acid (EACA) for dental extractions in hemophiliacs.

The results of a double-blind controlled trial, previously reported, showed that EACA is a useful adjunct to preoperative therapeutic concentrates of factor VIII or IX for dental extractions in hemophilia and Christmas disease. To estimate the amount of factor VIII and IX conserved in hemophiliacs receiving EACA for dental surgery compared with those not receiving EACA we have surveyed the usage of therapeutic materials in ten hemophilia centers in the U.S. and at Oxford. The amount of postoperative factor-VIII containing materials given to 20 U.S. hemophiliacs not receiving EACA averaged 11 062 units of factor-VIII activity per patient; 4,146 units for each of 22 U.S. patients receiving EACA; and 717 units for each of 56 patients at Oxford receiving EACA. Conservation of factor-IX-containing material was not as great. At Oxford 62.5% of patients receiving preoperative factor-VIII or -IX concentrates sufficient to raise the deficient factor to 50% of normal together with EACA, 24 g per day for ten days, required no postoperative therapeutic materials to control bleeding. The remainder required an average of two postoperative doses to control bleeding.

Adult↗
PubMed1975

A multicenter double blind clinical trial on 3.4.5-trimethoxybenzoiyl-epsilon-aminocaproic acid (C-3) in acute myocardial infarction.

186 out of 391 patients with acute myocardial infarction were treated with C-3 and 205 with placebo in a multicenter, double-blind clinical trial. Ensuing complications were treated in the same way in both groups. C-3 was injected i.v. slowly at the dose of 2 g statim plus 6 g by continuous drip infusion over 24 hrs for 5 days. During treatment, clinical progress was influenced only in regard to cardiac failure since in the C-3 group the improvement was more significant than in the placebo one (P less than 0.0025). Mortality rates were 8.1% and 11.2% for the C-3 and placebo groups, respectively. The difference in mortality was significant (P less than 0.05) for patients treated with C-3 for more than 24 hours. Mortality in male patients treated with C-3 for more than 12 hours was significantly lower (P less than 0.025). In patients less than 60 years old mortality rate was significantly lower (P less than 0.05) and was more so in patients receiving C-3 for more than 12 hours (P less than 0.025). Mortality due to complications was lower in the C-3 group, with arrhythmias (9.8% vs 14.2%), cardiogenic shock (69.2% vs 75%), and cardiac failure (9% vs 19.4%). Results agree with the hypothesis that C-3 may be effective in acute myocardial infarction by improving the action of traditional antiarrhythmic drugs, and augmenting myocardial contraction energy.

Acute Disease↗