This product belongs to Class III antiarrhythmic drugs. The main electrophysiological effect is to prolong the action potential and effective refractory period of various myocardial tissues, which is conducive to eliminating reentrant excitation. It also has mild non-competitive α and β adrenergic receptor blocking and mild Class I and IV antiarrhythmic properties. Reduce the automaticity of the sinus node. It has no effect on the resting membrane potential and action potential height. The inhibition of forward conduction of the atrioventricular bypass pathway is greater than the reverse. Due to excessive prolongation of repolarization, the electrocardiogram after oral administration has a prolonged QT interval and T wave changes, which can slow the heart rate by 15~20% and prolong the PR and Q-T intervals by about 10%. It has a direct dilation effect on the coronary arteries and peripheral blood vessels. It can affect thyroid hormone metabolism.

H2 receptor inhibitor, which has the effect of inhibiting gastric acid secretion. It is rapidly absorbed through the gastrointestinal tract after oral administration.

The anti-epileptic effect may be related to the competitive inhibition of γ-aminobutyric acid transferase, which reduces its metabolism and increases the content of γ-aminobutyric acid in the brain. It has different degrees of antagonism to convulsions caused by various factors.

The anti-epileptic effect may be related to the competitive inhibition of γ-aminobutyric acid transferase, which reduces its metabolism and increases the content of γ-aminobutyric acid in the brain. It has different degrees of antagonism to convulsions caused by various factors.

1. Positive inotropic effect: selectively inhibits the activity of Na--KATPase in myocardial cell membrane, increases the concentration of Ca2 in myocardial cells, and enhances myocardial contractility; 2. Negative frequency effect: improves hemodynamic state and slows down heart rate; 3. Cardiac electrophysiological effect: reduces the autonomy of sinoatrial node, improves the autonomy of Purkinje fibers, slows down the conduction velocity of atrioventricular node, and shortens the effective refractory period of atria and Purkinje fibers.

It can inhibit the metabolism of phenytoin, phenobarbital, primidone, and clonazepam, easily causing them to be poisoned; drinking alcohol can aggravate the sedative effect; combined use with anticoagulants (such as warfarin or heparin) and thrombolytics increases the risk of bleeding; combined use with aspirin or dipyridamole prolongs bleeding time; combined use with carbamazepine accelerates drug metabolism, and the blood drug concentration needs to be monitored to adjust the dosage; combined use with haloperidol, loxapine, maprotiline, monoamine oxidase inhibitors, phenothiazines, thioxanthenes and tricyclic antidepressants may increase the inhibition of the central nervous system, lower the convulsion threshold and the effect of valproic acid, and the dosage needs to be adjusted in time to control seizures.