The results of animal studies show that sodium ferulate can inhibit the production of malondialdehyde and thromboxane B2, reduce myocardial edema and the release of lactate dehydrogenase, and promote the production of 6-keto-prostaglandin F1α, and has anti-platelet aggregation, vasodilation and myocardial protection effects.

The antiasthmatic effect is similar to that of theophylline, and the cardiac stimulant effect is only 1/20~1/10 of that of aminophylline. It has less effect on the heart and nervous system and is suitable for asthma patients with tachycardia. It has a direct relaxant effect on the smooth muscle of the respiratory tract, partly by inhibiting phosphodiesterase to increase intracellular cAMP, and releasing endogenous adrenaline and norepinephrine to achieve bronchial dilation. At the same time, theophylline is a purine receptor blocker that can counteract the contractile effect of adenine on the respiratory tract, and can also enhance the contractility of the diaphragm and improve respiratory function.

It combines with pyrophosphate in the body to form a coenzyme, participates in the oxidative decarboxylation reaction of pyruvate and a-ketoglutaric acid in sugar metabolism, and is necessary for sugar metabolism. When it is deficient, oxidation is blocked to form pyruvate and lactic acid accumulation, which affects the body's energy supply, leading to symptoms of the nervous and cardiovascular systems, such as multiple peripheral neuritis (paresthesia, neuralgia, limb weakness, muscle soreness and atrophy, etc.), cardiovascular manifestations include dilation of small arteries, decreased diastolic blood pressure, myocardial metabolic disorders, palpitations, shortness of breath, chest tightness, cardiac hypertrophy, etc., and digestive tract manifestations include decreased appetite, weakness and weight loss, etc.

This product has the effect of inhibiting platelet aggregation caused by TXA2 (thromboxane A2); it can reduce the specific viscosity of whole blood and plasma, accelerate the electrophoresis of red blood cells, relax vascular smooth muscle, and increase coronary blood flow; it has a significant protective effect on myocardial ischemia.

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; they dilate the main coronary arteries and arterioles in normal and ischemic parts of the heart, antagonize spontaneous or ergonovine-induced coronary artery spasm, increase myocardial oxygen delivery in patients with coronary artery spasm, relieve and prevent coronary artery spasm; they reduce total peripheral resistance and myocardial oxygen consumption; they reduce the influx of calcium ions, prolong the effective refractory period of the atrioventricular node, and slow down conduction.