Furosemide

Absorption

Following oral administration, furosemide is absorbed from the gastrointestinal tract. It displays variable bioavailability from oral dosage forms, ranging from 10 to 90%. The oral bioavailability of furosemide from oral tablets or oral solution is about 64% and 60%, respectively, of that from an intravenous injection of the drug.

Toxicity

Clinical consequences from overdose depend on the extent of electrolyte and fluid loss and include dehydration, blood volume reduction, hypotension, electrolyte imbalance, hypokalemia, hypochloremic alkalosis, hemoconcentration, cardiac arrhythmias (including A-V block and ventricular fibrillation). Symptoms of overdose include acute renal failure, thrombosis, delirious states, flaccid paralysis, apathy and confusion. In cirrhotic patients, overdosage might precipitate hepatic coma.
In rats, the oral LD50, intraperitoneal LD50, and subcutaneous LD50 is 2600 mg/kg, 800 mg/kg, and 4600 mg/kg, respectively. The Lowest published toxic dose (TDLo) in a female is 6250 μg/kg.

Description

Furosemide (Item No. 26298) is an analytical reference standard categorized as a diuretic. Formulations containing diuretics, including furosemide, have been misused in sports for weight reduction and as masking agents in humans and to prevent exercise-induced pulmonary hemorrhage in racehorses. This product is intended for use in analytical forensic applications. This product is also available as a general research tool .

The Uses of Furosemide

Furosemide inhibits ion co-transport in the kidney. Furosemide is used as a diuretic.

Background

Furosemide is a potent loop diuretic that acts on the kidneys to ultimately increase water loss from the body. It is an anthranilic acid derivative. Furosemide is used for edema secondary to various clinical conditions, such as congestive heart failure exacerbation, liver failure, renal failure, and high blood pressure. It mainly works by inhibiting electrolyte reabsorption from the kidneys and enhancing the excretion of water from the body. Furosemide has a fast onset and short duration of action and has been used safely and effectively in both pediatric and adult patients. The use of furosemide is particularly beneficial in clinical settings that require a drug with a higher diuretic potential. In addition to oral formulations, the solution for intravenous and intramuscular administration is also available, which is typically limited to patients who are unable to take oral medication or for patients in emergency clinical situations.

What are the applications of Application

Furosemide is an inhibitor of NKCC and a GABAA receptor antagonist

Indications

Furosemide is indicated for the treatment of edema associated with congestive heart failure, cirrhosis of the liver, and renal disease, including the nephrotic syndrome, in adults and pediatric patients.
Oral furosemide is indicated alone for the management of mild to moderate hypertension or severe hypertension in combination with other antihypertensive medications.
Intravenous furosemide is indicated as adjunctive therapy in acute pulmonary edema when a rapid onset of diuresis is desired.
Subcutaneous furosemide is indicated for the treatment of congestion due to fluid overload in adults with NYHA Class II/III chronic heart failure. This drug formulation is not indicated for emergency situations or in patients with acute pulmonary edema.

Pharmacokinetics

Furosemide manages hypertension and edema associated with congestive heart failure, cirrhosis, and renal disease, including the nephrotic syndrome. Furosemide is a potent loop diuretic that works to increase the excretion of Na+ and water by the kidneys by inhibiting their reabsorption from the proximal and distal tubules, as well as the loop of Henle. It works directly acts on the cells of the nephron and indirectly modifies the content of the renal filtrate. Ultimately, furosemide increases the urine output by the kidney. Protein-bound furosemide is delivered to its site of action in the kidneys and secreted via active secretion by nonspecific organic transporters expressed at the luminal site of action.
Following oral administration, the onset of the diuretic effect is about 1 and 1.5 hours , and the peak effect is reached within the first 2 hours. The duration of effect following oral administration is about 4-6 hours but may last up to 8 hours. Following intravenous administration, the onset of effect is within 5 minutes, and the peak effect is reached within 30 minutes. The duration of action following intravenous administration is approximately 2 hours. Following intramuscular administration, the onset of action is somewhat delayed.

Metabolism

The metabolism of furosemide occurs mainly in the kidneys and the liver, to a smaller extent. The kidneys are responsible for about 85% of total furosemide total clearance, where about 40% involves biotransformation. Two major metabolites of furosemide are furosemide glucuronide, which is pharmacologically active, and saluamine (CSA) or 4-chloro-5-sulfamoylanthranilic acid.