论文部分内容阅读
本文综述了近年来关于急性心肌缺血后高 FFA 血症的发生、有害作用以及抗高 FFA 血症的措施等主要进展情况。急性心肌缺血后,血中 FFA 迅速升高,而高 FFA 血症可加重心肌缺血程度、扩大梗塞范围、减弱心肌收缩功能,并且还可能引起严重心律失常。其作用机制一般认为是:FFA 可导致酸中毒,并和心肌细胞内阳性离子结合形成皂盐,破坏生物膜,降低细胞内 Ca~(++)、Mg~(++)离子的浓度;此外,继发性脂酰 CoA 在细胞内堆聚可抑制各种有关代谢酶。近来证明:通过改善 FFA 代谢、抑制 FFA 升高,对减轻心肌缺血损害,改善心肌收缩功能以及降低心律失常发生率均取得较好效果,从而为防治急性心肌梗塞及其并发症方面开辟了一个新途径。
This review summarizes the major advances in recent years on the occurrence and adverse effects of hyperfibrinogenemia and antifungal hyperfunctions after acute myocardial ischemia. After acute myocardial ischemia, the blood FFA increased rapidly, while hyperfibrinogenemia may increase myocardial ischemia, expand the infarct size, reduce myocardial contractility, and may also cause serious arrhythmia. Its mechanism of action is generally believed to be: FFA can lead to acidosis, and myocardial cells and positive ions combine to form soap salts, destroy the biofilm, reduce intracellular Ca ~ (++), Mg ~ (++) ion concentration; In addition , Secondary fatty acyl CoA in the cell accumulation can inhibit a variety of metabolic enzymes. Recently, it has been proved that improving FFA metabolism and inhibiting the increase of FFA have good effect on alleviating myocardial ischemic damage, improving myocardial contractile function and reducing the incidence of arrhythmia, thus opening up one for prevention and treatment of acute myocardial infarction and its complications New way.