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Pharmacotherapeutic Group: Capillary-stabilising agents. ATC Code: C05CA.
Pharmacology: Pharmacodynamics: The target site of amorphous aescin is the vascular wall. In pathologically raised permeability, amorphous 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, amorphous aescin raises capillary resistance, inhibits inflammatory processes and improves microcirculation.
Pharmacokinetics: The metabolism of orally administered amorphous aescin was studied in rats and mice. After oral administration of tritium-marked amorphous aescin, the administered activitiy absorbed from the gastrointestinal tract averaged 12-16%. Excretion occurs by both bile and urine. The rate of metabolisation is bigger following oral administration than with IV application. The organ distribution of amorphous aescin is insignificant in the excretion organs liver and kidneys, compared to the increased blood level.
Toxicology: Humans: Acute Toxicity: The acute IV toxicity of aescin varies among species between 2-15.2 mg/kg. Toxicity due to acute nephrotic conditions can precipitate the clinical picture of fatal uraemia within 24-48 hrs.
Chronic Toxicity: Late toxicity has never been observed. β-aescin is tolerated very well by humans. The differences in toxicity between aescin and total horse chestnut extracts are of minor importance. The therapeutic window cannot be increased by freedom from saponins.
