Mildronate (also known as THP, MET-88 and mildronate) is a new type of heart protective drug. It is a compound with brand-new structure first developed by the Institute of organic synthesis in Latvia. It was first listed and sold in the former Soviet Union by grindeks company in 1989. At present, it is listed in 15 countries such as Latvia, Russia, Ukraine, Belarus, Azerbaijan, Armenia, Moldova and Lithuania. It is a structural analogue of carnitine, It can compete with carnitine γ- Trimethylaminobutyric salt hydroxylase can reduce the concentration of free carnitine and long-chain acetylcarnitine in cells, so it can inhibit the carnitine dependent fatty acid oxidation process. At present, there are the following types of drugs commonly used in clinic to treat myocardial ischemia: nitrates β Receptor blockers, calcium channel blockers and hypolipidemic drugs. Their main mechanism is to relax vascular smooth muscle, dilate vascular smooth muscle and coronary artery, reduce myocardial oxygen consumption and blood lipid. The mortality rate of patients with coronary heart disease remains high. The metabolic disorder during myocardial ischemia-reperfusion has been highly concerned by medical workers. In recent years, the role of drugs to improve myocardial metabolism in anti myocardial ischemia-reperfusion injury has attracted the attention of many scholars. Mitrozid acts on mitochondria and improves myocardial energy metabolism at the cellular level. In view of the obvious difference between these drugs and other anti myocardial ischemia drugs, they are also called cellular anti ischemia drugs.
1. Mildronate can improve the energy metabolism process of cardiomyocytes, inhibit carnitine dependent fatty acid oxidation, strengthen intracellular glucose metabolism, provide energy to tissues through anaerobic fermentation, and improve the symptoms of myocardial ischemia and hypoxia. It can be used in combination with other drugs (such as vasodilators, diuretics, etc.) in the treatment of ischemic heart disease.
2. Mildronate can promote the redistribution of blood in the ischemic areas of the heart and brain, and can be used in the treatment of various acute and chronic cerebral blood supply disorders.
3. By improving the process of fat metabolism, the drug can improve people's working ability and alleviate psychological and physiological excessive tension syndrome. Athletes taking the drug during training and competition can improve sports performance.
4. It can eliminate the functional damage to the nervous system of patients with chronic alcoholism during the onset of withdrawal syndrome. In addition, the drug can also improve the retinal vascular disease caused by nutritional disorders.
5. Membrane protection: cardiac ischemia causes the tension reaction of cardiomyocytes, which increases the decomposition of fatty acids in mitochondria, the accumulation of fatty acid metabolites in cells, the destruction of cell membrane devices and the increase of intracellular Ca + +. 6. Chemical book of energy optimization: midroxazide can reduce the accumulation of long-chain acyl carnitine, thus inhibiting carnitine dependent fatty acid oxidation, transforming the energy metabolism of hypoxic myocardium from fatty acid oxidation to more favorable glucose oxidation, that is, promoting the anaerobic oxidation of glycolysis pathway. Therefore, this product has anti hypoxia effect and cardioprotective activity.
7. Effect on energy metabolism enzymes: midroxazide can also prevent isoproterenol induced enhanced blood lactate dehydrogenase (myocardial specific isozyme) liver heteroactivity and prevent the increase of creatine phosphokinase activity.
8. Effect on carnitine excretion: other studies have shown that in addition to competitively inhibiting butyrate betaine hydroxylase and blocking the biosynthesis of carnitine, midrohydrazine also competitively affects the reabsorption of carnitine in the kidney.
9. Protection of ischemic heart: in the area of myocardial ischemia, the blocked anterior descending branch not only reduces ATP, ADP and muscle phosphate at the tissue level, but also increases amp and lactate at the tissue level, reducing the value of energy charge potential. The results showed that midroxazide could inhibit the of fatty acids β- Oxidation is very beneficial to the energy metabolism of ischemic myocardium.
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