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镁是许多酶的重要活化剂,特别是那些与三磷酸腺苷代谢有关的酶。已证明心脏组织中镁与肌原纤维中ATP的水解、肌凝蛋白凝胶体的超速沉着和脱水凝固作用、肌管反应中钙的结合与释放均为心肌收缩所必须。镁也兴奋心肌线粒体的氧化磷酸化作用,影响细胞膜的钠-钾-三磷酸腺苷酶及激活心脏内环化腺苷酶。近年来的文献综述已有大量证据说明镁与动物心脏病有关。很多研究显示当造成动物实验性缺氧时,镁从心脏中迅速丧失。缺镁饮食通常产生动物心肌代谢的改变,造成动物心肌纤维进行性坏死。多数研究证明,死于心肌梗塞患者的心肌中镁浓度减少,无论在梗塞区或非梗塞区镁浓度均减少,但死于慢性心脏病者心肌镁浓度未见减少,这些事实说明患者心肌内镁浓度低于正常的心肌梗塞者更易突然死亡。这
Magnesium is an important activator of many enzymes, especially those associated with adenosine triphosphate metabolism. It has been demonstrated that ATP is hydrolyzed in magnesium and myofibrils in cardiac tissues, and the fast calm and dehydration coagulation of myosin gel and the binding and release of calcium in myotubes are necessary for myocardial contraction. Magnesium is also excited myocardial oxidative phosphorylation of mitochondria, affecting the membrane of sodium - potassium - adenosine triphosphatase and activation of intracellular cyclic adenosine enzyme. Literature review in recent years There is a lot of evidence that magnesium and animal heart disease. Numerous studies have shown that magnesium rapidly loses from the heart when it causes experimental hypoxia in animals. Magnesium deficiency diet usually produces changes in myocardial metabolism, causing myocardial necrosis of myocardial fibers. Most studies have shown that myocardial magnesium in patients with myocardial infarction decreased in the concentration of magnesium, both in the infarction area or non-infarction area magnesium concentration decreased, but died of chronic heart disease, myocardial magnesium concentration was not reduced, these facts show that patients with intramyocardial magnesium Concentrations lower than normal myocardial infarction are more likely to die suddenly. This