Inhibit platelet aggregation and prevent thrombosis; counteract vascular damage caused by serotonin and bradykinin, increase capillary resistance, reduce capillary permeability, and prevent edema caused by increased vascular permeability.

Inhibit platelet aggregation and prevent thrombosis; counteract vascular damage caused by serotonin and bradykinin, increase capillary resistance, reduce capillary permeability, and prevent edema caused by increased vascular permeability.

This product is a dihydropyridine calcium channel blocker that inhibits transmembrane calcium influx in vascular smooth muscle and myocardium, but mainly acts on blood vessels, so it has strong vascular selectivity. It causes dilation of systemic blood vessels such as coronary arteries and renal arterioles, producing a hypotensive effect.

This product is an acidic polysaccharide drug with strong dispersing and emulsifying properties, improving the viscoelasticity of blood rheology, and an anticoagulant effect equivalent to 1/3 to 1/2 of heparin. It prevents platelet adhesion to collagen and inhibits platelet aggregation. It has prostaglandin (PGI2)-like effects such as anti-thrombotic, blood viscosity reduction, micro-arteriovenous spasm relief, and red blood cell and platelet depolymerization. It can also significantly reduce blood lipids, cholesterol, triglycerides, low-density lipoprotein (LDL), and very low-density lipoprotein (VLDL), increase high-density lipoprotein (HDL), and inhibit the occurrence and development of atherosclerotic lesions. It has a significant dilating effect on peripheral blood vessels, improves microcirculation, and inhibits the formation of thrombi in arteries and veins. It also has multiple functions such as lowering blood sugar and blood pressure.

By blocking the membrane transport of calcium ions in myocardial and vascular smooth muscle, inhibiting the influx of calcium ions into cells, it causes a decrease in myocardial contractility and vasodilation. Animal experiments have shown that by reducing myocardial contractility and peripheral vascular resistance, myocardial oxygen consumption is reduced; by dilating coronary vessels and developing collateral circulation, the oxygen supply to myocardial ischemic sites is increased; by inhibiting the consumption of high-energy phosphate compounds, the ability to resist hypoxia is enhanced.