Shanghai Harvest Pharmaceutical Co., Ltd.

This product is an α-adrenaline receptor agonist. This product is a sympathomimetic amine that acts directly on the receptors, but sometimes it also works indirectly by promoting the release of norepinephrine from the storage site. It acts on α receptors (especially the skin, mucous membranes, internal organs, etc.), causing vasoconstriction, increased peripheral resistance, and increased systolic and diastolic blood pressure. As blood pressure rises, it can stimulate the vagus nerve reflex and slow the heart rate, thereby treating supraventricular tachycardia. This product has a longer vasoconstrictive effect than adrenaline or ephedrine, and rarely causes central nervous system excitation at therapeutic doses; this product reduces blood flow to the kidneys, internal organs, skin and limbs, but increases coronary blood flow. As a vasoconstrictor, adding local anesthetic solution can slow down the latter's absorption, thereby limiting the scope of local anesthesia and prolonging its duration.

It can stimulate the carotid sinus and aortic body chemoreceptors (both are N19 receptors), reflexively excite the respiratory center and speed up breathing, but it has no direct excitation effect on the respiratory center. It also has a reflex excitation effect on the vagus nerve center and vasomotor center; it first excites the autonomic ganglia and then blocks them.

As a histamine H1 receptor antagonist, this product can counteract the capillary dilation caused by allergic reactions, reduce the permeability of capillaries, and relieve wheezing caused by bronchial smooth muscle contraction. This product has a long-lasting antihistamine effect and also has a significant central inhibitory effect, which can increase the effects of anesthetics, analgesics, hypnotics and local anesthetics. This product is mainly metabolized in the liver.

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.