This product is a histamine H2 receptor blocker. It has a significant inhibitory effect on gastric acid secretion, and can also inhibit the secretion of pepsin, and has a certain protective effect on animal experimental ulcers. It takes effect about 1 hour after taking the medicine, and the effect can last for more than 12 hours.

1. Increase the effect of anticoagulants; 2. Increase the level of phenytoin sodium in the blood; 3. Anticonvulsants such as carbamazepine and phenytoin sodium accelerate its metabolism and can displace thyroxine from plasma proteins; 4. The dosage of cardiac glycosides needs to be adjusted when used with cardiac glycosides; 5. Increase the effect of sympathomimetic drugs; 6. Increase the sensitivity of catecholamine receptors, thereby increasing the response of tricyclic antidepressants; 7. Cholestyramine reduces its absorption, and its dosage needs to be increased when using oral contraceptives at the same time.

It inhibits the demethylation of 14alpha-sterol mediated by cytochrome P450 in fungi, thereby inhibiting the biosynthesis of ergosterol. It has antibacterial activity against Candida species (including fluconazole-resistant strains of Candida krusei, Candida glabrata, and Candida albicans), bactericidal activity against all tested Aspergillus species, and also bactericidal activity against other pathogenic fungi, including Actinomyces and Fusarium species.

Sodium nitroprusside is a fast-acting and short-acting vasodilator. It has a direct dilating effect on both arterial and venous smooth muscles, but does not affect the contraction of the uterus, duodenum or myocardium. Vasodilation reduces peripheral vascular resistance, thus having a hypotensive effect. Vasodilation reduces both the preload and afterload of the heart and improves cardiac output, so it is beneficial for heart failure. Reducing afterload can reduce the impedance of the aorta and left ventricle during valvular insufficiency and reduce reflux.

Selective (cardioselective) β1 adrenergic receptor blocker, with rapid onset, short duration of action, and no obvious intrinsic sympathomimetic activity or membrane stabilizing effect at therapeutic doses. The elimination half-life after intravenous injection is about 9 minutes. It mainly inhibits β1 adrenergic receptors located in the myocardium, and in large doses also has a blocking effect on β2 adrenergic receptors in tracheal and vascular smooth muscle.