This product is a coenzyme that improves the body's metabolism and participates in the metabolism of fat, protein, sugar, nucleic acid and nucleotides in the body. It is also the main source of energy in the body. When energy is needed for absorption, secretion, muscle contraction and biochemical synthesis reactions in the body, adenosine triphosphate is decomposed into adenosine diphosphate and phosphate groups, and energy is released at the same time. Animal experiments have shown that this product can inhibit the slow calcium ion influx of slow-reacting fibers, block or delay the forward conduction in the atrioventricular node reentry pathway, and a large dose may also block or delay the forward and reverse conduction of the bypass; in addition, it also has a short-term and strong effect of enhancing the vagus nerve, thereby terminating arrhythmias caused by atrioventricular node reentry and bypass reentry mechanisms.

This product is an amide local anesthetic, which has a biphasic effect of excitation and inhibition on the central nervous system; at low doses, analgesia and drowsiness occur, and the pain threshold increases; when the dose is increased, the effect or toxicity increases, and it has an anticonvulsant effect at sub-toxic blood concentrations; convulsions may occur when the blood concentration is too high. At low doses, it can promote the outflow of K in myocardial cells, reduce myocardial autonomy, and have an anti-ventricular arrhythmia effect; at therapeutic doses, it has no significant effect on myocardial cell electrical activity, atrioventricular conduction, and myocardial contraction; when the blood concentration increases, it can cause a slowing of cardiac conduction velocity, atrioventricular conduction block, inhibition of myocardial contractility, and a decrease in cardiac output.

This product is an amide local anesthetic. After blood absorption or intravenous administration, it has obvious biphasic effects of excitation and inhibition on the central nervous system, and there may be no precursor excitation. When the blood concentration is low, analgesia and drowsiness occur, and the pain threshold increases; with increasing doses, the effect or toxicity increases, and it has an anticonvulsant effect at sub-toxic blood concentrations; convulsions may occur when the blood concentration exceeds 5μg·ml-1. At low doses, it can promote the outflow of K in myocardial cells, reduce the autonomy of the myocardium, and have an anti-ventricular arrhythmia effect; at therapeutic doses, it has no obvious effect on the electrical activity of myocardial cells, atrioventricular conduction, and myocardial contraction; further increases in blood concentrations can cause a slowing of the heart conduction velocity, atrioventricular conduction block, inhibition of myocardial contractility, and a decrease in cardiac output.

Specific pharmacological effects not provided

Anti-myocardial ischemia, improve hemodynamics, improve blood rheology, other effects (alleviate liver damage)

Anti-myocardial ischemia, improve hemodynamics, improve blood rheology, other effects (alleviate liver damage)

1. Anti-myocardial ischemia: Intravenous injection of 0.8, 1.6, and 3.2 g/kg of this product can reduce the scope of myocardial infarction in dogs with acute myocardial ischemia caused by ligation of the left anterior descending coronary artery, slow down the acceleration of heart rate caused by ischemia, reduce the release of CK, LDH, and MDA in serum, and enhance SOD activity. 2. Effect on hemodynamics: Intravenous injection of 0.26, 0.78, and 2.34 g/kg of this product can significantly increase the coronary flow and cardiac output of anesthetized dogs, reduce femoral artery systolic pressure (SAP), diastolic pressure (DAP), and mean arterial pressure (MAP). 3. Improve blood rheology: Intravenous injection of 4 g/kg of this product can significantly reduce the whole blood viscosity, hematocrit, and platelet aggregation of rats with blood stasis syndrome caused by intravenous injection of glucose saline, and increase the maximum deformation coefficient of red blood cells. 4. Other effects Oral administration of 0.4 and 0.8 g/kg of this product can reduce experimental liver damage in mice caused by galactosamine, reduce the levels of plasma and liver homogenate peroxide (LPO) and malondialdehyde (MDA), and reduce the levels of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST).

1. Anti-myocardial ischemia: Intravenous injection of 0.8, 1.6, and 3.2 g/kg of this product can reduce the scope of myocardial infarction in dogs with acute myocardial ischemia caused by ligation of the left anterior descending coronary artery, slow down the acceleration of heart rate caused by ischemia, reduce the release of CK, LDH, and MDA in serum, and enhance SOD activity. 2. Effect on hemodynamics: Intravenous injection of 0.26, 0.78, and 2.34 g/kg of this product can significantly increase the coronary flow and cardiac output of anesthetized dogs, reduce femoral artery systolic pressure (SAP), diastolic pressure (DAP), and mean arterial pressure (MAP). 3. Improve blood rheology: Intravenous injection of 4 g/kg of this product can significantly reduce the whole blood viscosity, hematocrit, and platelet aggregation of rats with blood stasis syndrome caused by intravenous injection of glucose saline, and increase the maximum deformation coefficient of red blood cells. 4. Other effects Oral administration of 0.4 and 0.8 g/kg of this product can reduce experimental liver damage in mice caused by galactosamine, reduce the levels of plasma and liver homogenate peroxide (LPO) and malondialdehyde (MDA), and reduce the levels of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST).