It can simultaneously relax the coronary arteries in the normal blood supply area and the ischemic area, antagonize spontaneous or ergonovine-induced coronary artery spasm, increase the delivery of myocardial oxygen to patients with coronary artery spasm, and relieve and prevent coronary artery spasm. It can also inhibit myocardial contraction, reduce myocardial metabolism, and reduce myocardial oxygen consumption. On the other hand, it can relax peripheral resistance vessels, reduce peripheral resistance, reduce systolic and diastolic blood pressure, and reduce cardiac afterload. It can delay the sinus node function and atrioventricular conduction of the isolated heart; electrophysiological studies on whole animals and humans have not found that this product has the effect of delaying atrioventricular conduction, prolonging the recovery time of the sinus node, and slowing down the sinus node rate.

It has the effects of anti-platelet aggregation, dilating arterioles, improving microcirculation and promoting blood circulation and removing blood stasis. It also has the effect of disaggregating the aggregated platelets.

This product is an antifibrinolytic drug. It binds to the lysine binding sites on plasminogen and plasmin, inhibiting the binding of plasminogen to fibrin and preventing its activation, thereby inhibiting fibrinolysis. At high concentrations (100 mg/L), it directly inhibits the activity of plasmin and achieves a hemostatic effect.

This product is a non-steroidal anti-inflammatory drug with anti-inflammatory, analgesic and antipyretic effects. Its mechanism of action is not yet fully understood, but it may be mainly related to the inhibition of prostaglandin synthesis, mediator release of leukocytes and oxidative reactions of polymorphonuclear leukocytes.

Calcium blockers (also known as slow channel blockers or calcium antagonists) block the entry of calcium ions across the membrane into myocardial and vascular smooth muscle cells.