Pharmacotherapeutic group: Capillary-stabilising agents. ATC code: C05AC07.
Pharmacology: Pharmacodynamics: The target site of Aescin is the vascular wall. In pathologically raised permeability, Aescin inhibits exudation by reducing the extravasation of fluid into the tissue and accelerating the subsidence of oedema. The mode of action is based on changes in the permeability of the affected capillary walls. In addition, Aescin raises capillary resistance, inhibits inflammatory processes and improves microcirculation.
Pharmacokinetics: The metabolism of oral administered Aescin was studied in rats and mice. After oral administration of tritium-marked Aescin, the administered activity absorbed from the gastrointestinal tract averaged 12% to 16%. Excretion occurs by both, bile and urine. The rate of metabolisation is bigger following oral administration than with intravenous application. The organ distribution of Aescin is insignificant in the excretion organs liver and kidneys, compared to the increased blood level.
Toxicology: Preclinical Safety Data: Aescin has not been studied sufficiently in animal experiments. In the existing studies, however, it proved medium to highly toxic. Especially significant were nephrotoxic changes. The complete mutagenicity studies yielded no hint at mutagenic effects. Studies on carcinogenicity have not been performed. Aescin has not been studied sufficiently with respect to reproduction toxicity. In mice and rabbits, following oral Aescin administration, embryotoxic effects (reduced fetal weight, retarded ossification of the skeleton, embryo mortality with higher doses) occurred during the phase of organogenesis. Effects on the vitality of prenatally exposed young animals were not discovered.
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