Chengdu Brilliant Pharmaceutical Co., Ltd.

1. Positive inotropic effect: This product selectively binds to the Na-KATPase of the myocardial cell membrane and inhibits the activity of the enzyme, causing damage to the active coupled transport of Na-K inside and outside the myocardial cell membrane, and increasing the concentration of Na in myocardial cells, thereby activating the exchange of Na and Ca2 on the sarcolemma, increasing the amount of Ca2 in the cytoplasm, and increasing the Ca2 reserve in the sarcoplasmic reticulum. When the myocardium is excited, more Ca2 is released; the increase in the concentration of Ca2 in myocardial cells excites myocardial contractile proteins, thereby increasing myocardial contractility; 2. Negative frequency effect: Due to its positive inotropic effect, it increases the cardiac output of the failing heart, improves the hemodynamic state, eliminates the reflex increase of sympathetic nerve tension, and enhances the vagus nerve tension, thereby slowing down the heart rate and delaying atrioventricular conduction. In addition, at low doses, it increases the sensitivity of the sinoatrial node to vagus nerve impulses, which can enhance its effect of slowing down the heart rate. Due to its negative frequency effect, the diastole period is relatively prolonged, which is beneficial to increase myocardial blood supply; large doses (usually close to the toxic dose) can directly inhibit the sinoatrial node, atrioventricular node and His bundle to present sinus bradycardia and varying degrees of atrioventricular conduction block; 3 Cardiac electrophysiological effects: through direct effects on myocardial electrical activity and indirect effects on the vagus nerve, it reduces the autonomy of the sinoatrial node; improves the autonomy of Purkinje fibers; slows down the conduction velocity of the atrioventricular node, prolongs its effective refractory period, and leads to an increase in latent conduction of the atrioventricular node, which can slow down the ventricular rate of atrial fibrillation or atrial flutter; since this drug shortens the effective refractory period of the atrium, when used for atrial tachycardia and atrial flutter, it may lead to acceleration of the atrial rate and conversion of atrial flutter to atrial fibrillation; shortens the effective refractory period of Purkinje fibers.

This product is a vitamin drug. Vitamin K is a necessary substance for the liver to synthesize factors II, VII, IX, and X. Vitamin K deficiency can cause synthesis disorders or abnormalities of these coagulation factors, and clinically bleeding tendency and prolonged prothrombin time can be seen.

O-3-amino-3-deoxy-α-O-glucopyranosyl-(1→6)-O-[2,6-diamino-2,3,6-trideoxy-α-D-ribo-hexopyranosyl-(1→4)]-2-deoxy-D-streptamine. Molecular weight: C18H37N5O9