Description

Esafosfina 10 gr. vial

Esafosfina operates through cell wall interaction, boosting phosphofructokinase activity, elevating energy-rich phosphorus compound levels, and facilitating potassium ion influx.

In acute myocardial infarction patients, Esafosfina enhances hemodynamics, reduces myocardial necrosis size, increases cardiac index and stroke volume, and improves ECG readings.

Phosphate, vital for intracellular fluids, influences physiological processes, including ATP synthesis, oxygen transport, glycolysis, and pH regulation.

Normal adult phosphate levels range from 0.8 to 1.5 mmol/L. Hypophosphatemia is common in various clinical situations, impacting muscle function, metabolism, and respiratory capabilities.

Compatibility of fructose-1,6-diphosphate (FDP) with cations, especially calcium ions, in parenteral nutrition mixtures surpasses inorganic phosphates.

FDP’s rapid absorption and distribution yield a short plasma half-life of 10-15 minutes, effectively contributing to metabolic processes.

Esafosfina is characterized by its membrane-protective action, increasing potassium ion uptake by erythrocytes and lowering its plasma concentration. This leads to a higher intracellular to extracellular potassium ion ratio and pH values, counteracting acidosis.

Esafosfina influences cell oxygen supply. In vitro experiments reveal elevated ATP levels in human blood erythrocytes and enhanced oxygen transport through increased 2,3-DPG content (which directly affects erythrocyte oxygen levels).

Esafosfina can act as a stimulator of repolarization and glucose metabolism in smooth muscle cells, including myometrial cells, as it maintains a high intracellular potential (high ATP/ADP ratio). It contributes to increased phosphofructokinase activity, intracellular energy-rich phosphate compound stores, and potassium ion influx into cells. In fat cells, it prevents histamine release.

The medication triggers the restoration of nicotinamide adenine dinucleotide (NAD+), a coenzyme for cytoplasmic and mitochondrial alcohol dehydrogenases. These enzymes, in turn, oxidize ethanol to acetaldehyde and acetate, reducing its concentration.

Clinical studies have confirmed that esafosfina therapy rapidly and effectively increases 2,3-DPG levels in the blood. Since this therapy leads to a quick rise in oxygen concentration without increasing cardiac load, the medication can be indicated for use in critically ill patients requiring multiple transfusions.

The medication affects cellular membrane deformability, improving blood rheological properties, including erythrocyte flexibility and hemolysis resistance.

Contraindications

Hereditary fructose intolerance, hyperphosphatemia, renal failure, hypersensitivity.

Composition

Each vial contains 5 g D-fructose-1,6-diphosphate sodium salt hydrate (equivalent to 3.75 g D-fructose-1,6-diphosphoric acid). Diluent: water for injection.

Release Form

Lyophilized powder for infusion solution, complete with 50 ml solvent vial and infusion system.

Physical and Chemical Properties

Hygroscopic crystalline powder, reconstituted into a clear, colorless or light yellow liquid.

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[The effect of esafosfina on cerebral circulation in intact and ischemized rat brain]