Furosemid solution for injections ampoules 1% 2 ml. №10


Manufacturer: Ukraine

Edema in chronic congestive heart failure (if treatment with diuretics is necessary). Edema in chronic renal failure. Acute renal failure, including in pregnant women or during childbirth. Edema in nephrotic syndrome (if treatment with diuretics is necessary). Swelling in liver disease (if necessary to complement the treatment with the use of aldosterone antagonists). Arterial hypertension.



Furosemid Composition
active substance: furоsemide;

1 ml of solution contains 10 mg furosemide;

excipients: sodium chloride, sodium hydroxide, water for injection.

Furosemid Dosage form

Basic physical and chemical properties: transparent colorless or slightly yellowish liquid.

Furosemid Pharmacotherapeutic group
Highly active diuretics. Sulfonamide preparations. ATC code С03С А01.

Furosemide is a short-acting loop diuretic that produces a relatively strong and short-term diuretic effect. Furosemide blocks the Na + K + 2Cl-cotransporter, which is located in the basement membranes of the cells of the thick segment of the ascending part of Henle’s loop: the effectiveness of the saluretic action of furosemide, therefore, depends on whether the drug enters the tubules at the lumen 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 sodium glomerular filtration rate. Secondary effects of increased sodium excretion are increased urinary excretion (due to osmotically bound water) and increased distal tubular potassium secretion. The 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 suggests 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 relative to catecholamines, increased in patients with arterial 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 primarily as unchanged drug by secretion into the proximal tubule. After intravenous administration, 60 to 70% of the administered dose of furosemide is excreted in this way. The metabolite of furosemide – glucuronide – makes up 10-20% of the substances contained in the 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, through the placental barrier and slowly passes to the fetus. Furosemide is determined in the fetus or in newborns at the same concentrations as in the mother of the child.

Hypersensitivity to furosemide or to other components that make up the drug.
In patients who are allergic to sulfonamides (for example, sulfonamide antibiotics or sulfonylureas), cross-sensitivity to furosemide may occur.
Hypovolemia or dehydration of the body.
Renal failure in the form of anuria if there is no therapeutic response to furosemide.
Renal failure due to poisoning with nephrotoxic or hepatotoxic drugs.
Severe hypokalemia.
Severe hyponatremia.
Pre-coma or coma associated with hepatic encephalopathy.