Nonsteroidal anti-inflammatory drugs have analgesic, anti-inflammatory, antipyretic and platelet aggregation inhibitory effects. The specific mechanisms include: 1. Analgesic effect by inhibiting the synthesis of prostaglandins and other pain-causing substances; 2. Anti-inflammatory effect may be through inhibiting the synthesis of prostaglandins and inflammatory mediators; 3. Antipyretic effect may be through acting on the hypothalamic temperature regulation center; 4. Anti-rheumatic effect is mainly anti-inflammatory; 5. Inhibition of platelet aggregation by inhibiting cyclooxygenase to reduce prostaglandin production.

Calcium ion antagonists exert their pharmacological effects by regulating the influx of calcium ions on the cell membranes of myocardial conduction cells, myocardial contractile cells, and arterial smooth muscle cells; dilate the main coronary arteries and arterioles, antagonize coronary artery spasm, and increase myocardial oxygen delivery; reduce total peripheral resistance and lower myocardial oxygen consumption; reduce calcium ion influx, prolong the effective refractory period of the atrioventricular node, and slow conduction.

It has significant anti-coagulation factor Xa activity, and low anti-coagulation factor IIa or antithrombin activity (30 IU/ml). It can inhibit the formation of thrombi in vivo and in vitro and arteriovenous thrombi, but does not affect platelet aggregation and the binding of fibrinogen to platelets. When it exerts its antithrombotic effect, the possibility of bleeding is small. At the recommended dose for different indications, low molecular weight heparin does not prolong bleeding time. At the preventive dose, it does not significantly change APTT.