Mechanism of myocardial ischemia-reperfusion injury

Myocardial ischemia-reperfusion injury refers to the fact that the ischemic myocardium, after restoring blood reperfusion, instead aggravates its structural damage and causes cell death, resulting in the expansion of myocardial infarction, causing further damage to cardiac function and affecting the prognosis of patients with myocardial infarction. The causes are not fully understood, and the possible mechanisms are as follows: 1. calcium overload theory, the myocardium is like soil, after long-term ischemia and hypoxia, when reoxygenation or reperfusion, there is a large rush of extracellular calcium ions into the cells, resulting in intracellular calcium overload, which seriously affects the repair of damaged cells. 2. leukocyte infiltration theory, when the tissue is damaged, the cell membrane will be degraded, and the metabolites of arachidonic acid will increase, some of which The leukocyte infiltration theory, when the tissue is damaged, the cell membrane will be degraded and the arachidonic acid metabolites will increase, some of which have strong chemotactic effects, so they can attract a large number of leukocytes into the tissue or adhere to the vascular endothelium, while the leukocytes themselves can release many inflammatory mediators with chemotactic effects, which also aggravate the damage to the endothelium. 3, the free radical theory, due to excessive production of reactive oxygen species or reduced antioxidant enzyme activity, can trigger a chain of lipid peroxidation reaction, damage the cell membrane and then cell death, thus aggravating the damage to the myocardium. This aggravates myocardial damage.