Furosemide Injection

1 Effect on water and electrolyte excretion. It can increase the excretion of water, sodium, chloride, potassium, calcium, magnesium, phosphorus, etc. Unlike thiazide diuretics, loop diuretics such as furosemide have a clear dose-effect relationship. As the dose increases, the diuretic effect is significantly enhanced, and the drug dosage range is large. This type of drug mainly inhibits the active reabsorption of NaCl by the thick-walled segment of the renal tubular loop of Medullary. As a result, the concentrations of Na+ and Cl- in the tubular fluid increase, while the concentrations of Na+ and Cl- in the medullary interstitial fluid decrease, which reduces the osmotic pressure gradient difference and the tubular concentrating function decreases, resulting in increased excretion of water, Na+, and Cl-. Due to the decrease in Na+ reabsorption, the concentration of Na+ in the distal tubule increases, which promotes the increase of Na+-K+ and Na+-H+ exchange, and increases the excretion of K+ and H+. As for the mechanism by which furosemide inhibits the reabsorption of Cl- in the thick-walled segment of the ascending limb of the renal tubular loop, it was previously believed that there was a chloride pump in this area. Current studies have shown that there is a Na+ and Cl- paired transport system related to Na+-K+ ATPase on the outside of the basement membrane of this area. Furosemide reduces the reabsorption of Na+ and Cl- by inhibiting the function of this system. In addition, furosemide may also inhibit the reabsorption of Na+ and Cl- by the proximal and distal tubules and promote the secretion of K+ by the distal tubules. Furosemide increases the excretion of Ca2+ and Mg2+ by inhibiting the reabsorption of Ca2+ and Mg2+ by the loop of Henle. Short-term use of the drug can increase uric acid excretion, while long-term use can cause hyperuricemia. 2 Effects on hemodynamics. Furosemide can inhibit the activity of prostaglandin degrading enzymes, increase the content of prostaglandin E2, and thus have a vasodilatory effect. Dilation of renal blood vessels, reduction of renal vascular resistance, and increase of renal blood flow, especially deep renal cortical blood flow, are of great significance in the diuretic effect of furosemide and are also the theoretical basis for its use in preventing acute renal failure. In addition, unlike other diuretics, loop diuretics increase tubular fluid flow while the glomerular filtration rate does not decrease, which may be related to the reduction of chloride flowing through the macula densa, thereby weakening or blocking the glomerular-tubular balance. Furosemide can dilate pulmonary capacitance veins and reduce pulmonary capillary permeability. In addition, its diuretic effect reduces the amount of blood returning to the heart and reduces the left ventricular end-diastolic pressure, which is helpful for the treatment of acute left heart failure. Since furosemide can reduce pulmonary capillary permeability, it provides a theoretical basis for its treatment of adult respiratory distress syndrome.

Main ingredient: Furosemide. Chemical name: 2-[(2-furanylmethyl)amino]-5-(aminosulfonyl)-4-chlorobenzoic acid. Molecular formula: C12H11ClN2O5S Molecular weight: 330.74

This product is used for: 1. Edema diseases, including congestive heart failure, cirrhosis, kidney disease (nephritis, nephropathy and acute and chronic renal failure caused by various reasons), especially when other diuretics are ineffective, this type of drug may still be effective. Used in combination with other drugs to treat acute pulmonary edema and acute cerebral edema. 2. Hypertension. It is generally not the first choice for the treatment of primary hypertension, but when thiazide drugs are ineffective, especially when accompanied by renal insufficiency or hypertensive crisis, this type of drug is particularly suitable. 3. Prevention of acute renal failure. It is used for insufficient renal blood perfusion caused by various reasons, such as dehydration, shock, poisoning, anesthesia accidents and circulatory insufficiency. Timely application while correcting insufficient blood volume can reduce the chance of acute tubular necrosis.

1 Adults (1) Treatment of edema diseases. The initial dose is 20-40 mg orally, once a day. If necessary, an additional 20-40 mg can be added after 6-8 hours until a satisfactory diuretic effect occurs. Although the maximum dose can reach 600 mg per day, it should generally be controlled within 100 mg and taken in 2-3 times. To prevent excessive diuresis and adverse reactions. For some patients, the dose can be reduced to 20-40 mg, once every other day, or taken continuously for 2-4 days per week, 20-40 mg per day. (2) Treatment of hypertension. Start with 40-80 mg per day, divided into 2 doses, and adjust the dose as appropriate. (3) Treatment of hypercalcemia. Take 80-120 mg orally daily, divided into 1-3 doses. 2 Children's treatment of edema diseases, start with 2 mg based on body weight

Common symptoms are related to water and electrolyte disorders, especially when used in large doses or for long periods of time, such as postural hypotension, shock, hypokalemia, hypochloremia, hypochloremic alkalosis, hyponatremia, hypocalcemia, and related thirst, fatigue, muscle aches, arrhythmias, etc. Rare symptoms include allergic reactions (including rash, interstitial nephritis, and even cardiac arrest), blurred vision, xanthoopia, photosensitivity, dizziness, headache, anorexia, nausea, vomiting, abdominal pain, diarrhea, pancreatitis, muscle rigidity, bone marrow suppression leading to granulocytopenia, thrombocytopenic purpura and aplastic anemia, liver damage, paresthesia of fingers (toes), hyperglycemia, positive urine sugar, aggravation of existing diabetes, and hyperuricemia. Tinnitus and hearing impairment are more common when large doses are injected intravenously rapidly (doses greater than 4-15 mg per minute), and are mostly temporary, with a few being irreversible, especially when used simultaneously with other ototoxic drugs. In cases of hypercalcemia, it can cause kidney stones. There are also reports that this drug can aggravate idiopathic edema.

1. This drug can pass through the placental barrier. Pregnant women, especially those in the first three months of pregnancy, should avoid using it as much as possible. It has no preventive effect on pregnancy-induced hypertension syndrome. Animal experiments show that this product can cause fetal hydronephrosis, miscarriage and increased fetal mortality. 2. This drug can be secreted through breast milk. Women who are breastfeeding should use it with caution.

Precautions during pregnancy and lactation: Pregnant women, especially during the first 3 months of pregnancy, should avoid using it as much as possible, and lactating women should use it with caution.

1 Adrenal glucose, mineralocorticoids, adrenocorticotropic hormone and estrogen can reduce the diuretic effect of this drug and increase the chance of electrolyte disorders, especially hypokalemia. 2 Non-steroidal anti-inflammatory analgesics can reduce the diuretic effect of this drug and increase the chance of renal damage, which is related to the former inhibiting prostaglandin synthesis and reducing renal blood flow. 3 When used in combination with sympathomimetic drugs and anticonvulsant drugs, the diuretic effect is weakened. 4 When used in combination with clofibrate (clofibrate), the effects of both drugs are enhanced, and muscle soreness and stiffness may occur. 5 When used in combination with dopamine, the diuretic effect is enhanced. 6 Drinking alcohol, alcohol-containing preparations and drugs that can cause a drop in blood pressure can enhance the diuretic and hypotensive effects of this drug; when used in combination with barbiturates and anesthetics, it is easy to cause postural hypotension. 7 This drug can reduce uric acid excretion and increase blood uric acid, so when used in combination with drugs for the treatment of gout, the dose of the latter should be appropriately adjusted. 8 Reduce the efficacy of lowering blood sugar. 9 It reduces the effects of anticoagulants and antifibrinolytics, mainly due to the decrease in blood volume after diuresis, which leads to an increase in the concentration of coagulation factors in the blood, and the improvement of liver blood supply and increased synthesis of coagulation factors by diuresis. 10 This drug enhances the effect of non-depolarizing pine drugs, which is related to the decrease in blood potassium. 11 When used in combination with antibiotics such as amphotericin, cephalosporin, and aminoglycosides, nephrotoxicity and ototoxicity increase, especially when there is original renal damage. 12 When used in combination with antihistamines, ototoxicity increases, and tinnitus, dizziness, and vertigo are prone to occur. 13 The nephrotoxicity is obvious when used in combination with lithium, and it should be avoided as much as possible. 14 After taking chloral hydrate, intravenous injection of this drug can cause sweating, facial flushing, and increased blood pressure, which is related to the increase in thyroid hormone from a bound state to a free state, leading to enhanced decomposition. 15 When used in combination with sodium bicarbonate, the chance of hypochloremic alkalosis increases.

Keep away from light and store in sealed container.

2ml:20mg

Shanxi Guorun Pharmaceutical Co., Ltd.

• Founded in:

  2003-03-17

• Address:

  No. 6, Northwest Street, Yanggao County, Datong City, Shanxi Province

• Tax NO.:

  91140221746047833T

• Registered Funds:

  15 million yuan

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