A derivative of methylxanthine, it is a bronchodilator that can directly act on the bronchi and relax bronchial smooth muscles. It relaxes smooth muscles by inhibiting phosphodiesterase in smooth muscle cells, thereby suppressing asthma.

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 flow of renal tubular fluid 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.

Extract from the above information

This product is a non-steroidal anti-inflammatory drug. It has analgesic, anti-inflammatory and antipyretic effects in animal models, and its mechanism may be related to the inhibition of prostaglandin synthesis.

It is a prodrug of acetaminophen. After injection, it can be quickly hydrolyzed by plasma esterase to release acetaminophen to take effect. It produces analgesic effect by inhibiting arachidonic acid metabolism, inhibiting the production and release of endogenous pain-causing substances; selectively inhibiting the production of prostaglandins in the central nervous system, producing analgesic effects similar to morphine, and is used for postoperative analgesia. In addition, it has sedative and antipyretic effects, and is suitable for acute cases such as high fever and pain or patients who are not suitable for oral administration. There is no tolerance and dependence.