论文部分内容阅读
目前已有多种在缺血缺氧时保护心肌损伤的方法。其中有的旨在降低心肌代谢的能量需求,如低温、钾镁离子心脏瘫痪、钙离子拮抗剂及碱性溶液的应用等等,但此类方法在应用中受到明显限制。理想的方法是在低氧甚至无氧时满足心肌的能量需求。Lolley 及 Hewitt 曾证实了增加细胞内磷酸化葡萄糖可以改善或增强缺血后心肌的功能,本文经实验证实,在低氧、无氧时应用1,6-二磷酸果糖(FDP)可有效地改善心脏局部及整体的缺血,并对各种类型的休克均有裨益。FDP 应用的理论基础:缺血缺氧时,糖酵解增
There are many ways to protect myocardial injury during ischemia and hypoxia. Some of them are designed to reduce the energy requirements of myocardial metabolism such as hypothermia, paralysis of potassium and magnesium ions, application of calcium ion antagonists and alkaline solutions, etc. However, such methods are obviously limited in application. The ideal method is to meet the energy requirements of the myocardium in hypoxia or even oxygen free. Lolley and Hewitt have confirmed that increasing intracellular phosphorylated glucose can improve or enhance the function of ischemic myocardium. It has been experimentally demonstrated that hypoglycemic and anaerobic applications of fructose-1,6-diphosphate (FDP) can be effectively improved Local and global heart ischemia, and for all types of shock are beneficial. FDP application of the theoretical basis: ischemia and hypoxia, glycolysis increased