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It stimulates the adrenergic receptors of the sympathetic nervous system and the dopamine receptors located in the kidney, mesentery, coronary artery, and cerebral artery, and its effect is dose-dependent. At low doses (0.5-2μg/kg per minute based on body weight), it mainly acts on dopamine receptors, dilates the blood vessels of the kidney and mesentery, increases renal blood flow and glomerular filtration rate, and increases urine volume and sodium excretion; at small to medium doses (2-10μg/kg per minute based on body weight), it can directly stimulate β1 receptors and indirectly promote the release of norepinephrine from storage sites, produce positive stress on the myocardium, increase myocardial contractility and stroke volume, and ultimately increase cardiac output, systolic blood pressure, and possibly increase pulse pressure, with no change or slight increase in diastolic blood pressure, and peripheral total resistance often unchanged, and coronary blood flow and oxygen consumption improved; at high doses (more than 10μg/kg per minute based on body weight), it stimulates α receptors, resulting in increased peripheral vascular resistance, renal vasoconstriction, and reduced renal blood flow and urine volume. Due to the increase in cardiac output and peripheral vascular resistance, both systolic and diastolic blood pressures increase. (1) It stimulates the cardiac β1 receptors and has a much stronger effect on increasing myocardial contractility; (2) It increases the blood flow to the kidneys and mesentery, which can prevent the malignant development of shock caused by ischemia of these organs. Under the same condition of increasing myocardial contractility, the effects of causing arrhythmias and increasing myocardial oxygen consumption are weaker. In short, dopamine is particularly suitable for shock patients with weakened myocardial contractility, decreased urine output, and replenished blood volume.

Tetracycline antibiotics. This product is a broad-spectrum antibacterial agent. Many Rickettsia, Mycoplasma, Chlamydia, Spirochete, Amoeba and some Plasmodium are also sensitive to this product. Enterococcus is resistant to it. Others such as Actinomycetes, Bacillus anthracis, Listeria monocytogenes, Clostridium, Nocardia, Vibrio, Brucella, Campylobacter, Yersinia, etc. are sensitive to this product. This product has certain antibacterial activity against gonococci and meningococci, but penicillin-resistant gonococci are also resistant to oxytetracycline. Due to the widespread use of tetracyclines over the years, common clinical pathogens have serious resistance to oxytetracycline, including Gram-positive bacteria such as Staphylococcus and most Gram-negative bacteria. There is cross-resistance between different varieties of tetracycline antibiotics.

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 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.