edema in chronic heart failure; edema in chronic kidney failure; arterial hypertension; renal failure; acute renal failure, including during pregnancy or childbirth; edema of the lungs and brain; diuresis.
Lazix NEO Storage
active substance: furosemide;
1 ml of solution contains furosemide 10 mg;
Excipients: sodium hydroxide, sodium chloride, water for injections.
Lazix NEO Dosage form
Solution for injection.
Basic physical and chemical properties: transparent colorless solution that does not contain visible particles.
Lazix NEO Pharmacotherapeutic group
Highly active diuretics. Preparations of sulfamides.
ATX code C03C A01.
Lazix NEO Pharmacological properties
Furosemide is a fast-acting loop diuretic that has a relatively strong and short-term diuretic effect. Furosemide blocks the Na + K + 2Cl cotransporter located in the basement membranes of the cells of the thick segment of the ascending part of the Henle loop: the efficacy of the saluretic action of furosemide thus depends on whether the drug enters the tubules at the lumens by the anion transport mechanism. The diuretic effect occurs as a result of inhibition of sodium chloride reabsorption in this segment of the Henle loop. As a result, fractional sodium excretion can reach 35% of glomerular sodium filtration. Secondary effects of increased sodium excretion are increased urinary excretion (due to osmotically bound water) and increased distal tubular potassium secretion. Excretion of calcium and magnesium ions also increases. Furosemide causes dose-dependent stimulation of the renin-angiotensin-aldosterone system. In heart failure, furosemide leads to an acute decrease in cardiac preload (by narrowing the capacitive venous vessels). This early vascular effect is prostaglandin-mediated and involves adequate renal function with activation of the renin-angiotensin system and intact prostaglandin synthesis. In addition, due to its inherent natriuretic effect, furosemide reduces vascular reactivity to catecholamines, which is increased in patients with hypertension.
The volume of distribution of furosemide is from 0.1 to 0.2 liters per 1 kg of body weight. The volume of distribution may be higher depending on the disease.
Furosemide (more than 98%) forms strong compounds with blood plasma proteins, especially albumin.
Furosemide is excreted mainly as unchanged drug by secretion into the proximal tubule. After intravenous administration, from 60% to 70% of the administered dose of furosemide is excreted in this way. The metabolite of furosemide – glucuronide – is 10-20% of substances contained in urine. The residual dose is excreted in the feces, probably by biliary secretion.
The terminal half-life of furosemide after intravenous administration is approximately 1 to 1.5 hours.
Furosemide passes into breast milk, crosses the placental barrier and enters the fetus slowly. Furosemide is detected in the fetus or newborn in the same concentrations as in the mother of the child.
Edema in chronic congestive heart failure (if treatment with diuretics is required).
Edema in acute congestive heart failure.
Edema in chronic renal failure.
Acute renal failure, including in pregnant women or during childbirth.
Edema in liver disease (if necessary, to supplement treatment with aldosterone antagonists).
Hypertensive crisis (as a supportive tool).
Support of forced diuresis.