This product is a coenzyme that improves the body's metabolism and participates in the metabolism of fat, protein, sugar, nucleic acid and nucleotides in the body. It is also the main source of energy in the body. When energy is needed for absorption, secretion, muscle contraction and biochemical synthesis reactions in the body, adenosine triphosphate is decomposed into adenosine diphosphate and phosphate groups, and energy is released at the same time. Animal experiments have shown that this product can inhibit the slow calcium ion influx of slow-reacting fibers, block or delay the forward conduction in the atrioventricular node reentry pathway, and a large dose may also block or delay the forward and reverse conduction of the bypass; in addition, it also has a short-term and strong effect of enhancing the vagus nerve, thereby terminating arrhythmias caused by atrioventricular node reentry and bypass reentry mechanisms.

Converted into bicarbonate ions in the body to regulate acid-base balance and maintain normal physiological functions; lactate ions can correct metabolic acidosis and allow potassium ions to enter cells from blood and extracellular fluid.

Sodium is the most important cation in extracellular fluid and is the main substance for maintaining constant body fluid osmotic pressure and extracellular volume.

Potassium is the main intracellular cation and plays an important role in maintaining normal neuromuscular excitability.

Calcium ions act as second messengers in cells and are closely related to many functions of the body.

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The effect on water and electrolyte excretion is basically the same as furosemide, and its diuretic effect is 20 to 60 times that of furosemide. It mainly inhibits the active reabsorption of NaCl by the thick wall segment of the ascending limb of the renal tubular loop of Henle, and also inhibits the reabsorption of Na in the proximal tubule, but has no effect on the distal tubule, so the potassium excretion effect is less than furosemide. It 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 bumetanide, and are also the theoretical basis for its use in the prevention of acute renal failure. In addition, unlike other diuretics, loop diuretics increase the renal 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. Bumetanide can dilate the pulmonary capacitance veins and reduce the permeability of pulmonary capillaries. Its diuretic effect can reduce the amount of blood returning to the heart and the left ventricular end-diastolic pressure, which is helpful for the treatment of acute left heart failure. Since bumetanide can reduce the permeability of pulmonary capillaries, it provides a theoretical basis for its treatment of adult respiratory distress syndrome.

This product can cause blood vessels to contract, reduce capillary permeability, enhance platelet aggregation and adhesion, promote platelets to release coagulation active substances, shorten coagulation time, and achieve hemostatic effect.

It changes the neurotransmission of the brain, has an agonist effect on dopamine and 5-hydroxytryptamine receptors, has a blocking effect on α-adrenaline receptors, improves the damaged brain metabolic function, and shortens the brain circulation time. This effect is reflected in the change of brain electrical activity, and there are significant changes in the power spectrum of the electroencephalogram (EEG).