Читать книгу Manual of Equine Anesthesia and Analgesia - Группа авторов - Страница 319

 Furosemide is the most commonly used diuretic in horses.

 Furosemide inhibits the Na+‐K+‐Cl− cotransporter in the luminal membrane of the thick ascending limb of the LOH.It binds specifically and reversibly to the Cl− binding site of the transporter's transmembrane domain.

 Because this transporter reabsorbs about 25% of the sodium load, its inhibition by furosemide causes an increase in the distal tubular concentration of sodium, leading to a decrease in water reabsorption in the collecting duct.This inhibits reabsorption of Na+, Cl−, K+, and water.

 It blocks the ability of the kidney to develop a counter‐current mechanism, limiting the ability to concentrate or dilute urine.

 Furosemide induces renal synthesis of prostaglandins, and this increases RBF and leads to a redistribution of renal cortical blood flow.

 Furosemide reduces plasma and extracellular fluid volume resulting in decreased blood pressure and cardiac output.

 Its use can lead to volume depletion, azotemia, metabolic alkalosis, and electrolyte abnormalities (hyponatremia, hypokalemia).

 The loss of H+ and K+ can be attributed in part to activation of the RAAS secondary to a decrease in blood volume and pressure.Aldosterone causes sodium reabsorption and increases K+ and H+ excretion.

 Can potentiate the toxicity of aminoglycosides.