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目的:观察果糖二磷酸钠(FDP)对新生大鼠心肌缺氧缺血(HI)损伤的作用及其机制。方法:40只新生大鼠随机分为4组(每组10只):假手术组、HI组、FDP组和预使用FDP组,采用冠状动脉结扎和置缺氧箱的方法,制备大鼠在体心肌缺血缺氧损伤模型。分别测定血清氧化亚氮(NO)、丙二醛(MDA)、超氧化物歧化酶(SOD)和乳酸脱氢酶(LDH)水平,观察光镜及透射电镜下心肌结构病理变化。结果:HI组血清LDH(7789.36 U/L)、MDA(4.30μmol/L)水平明显高于假手术组(3608.47 U/L,1.76μmol/L)(P<0.01).NO(23.24μmol/L)、SOD(115.49 U/mL)低于假手术组(56.88μmol/L,239.52 U/mL)(P<0.01);FDP组和预使用FDP组血清LDH(4237.58 U/L和3600.82 U/L)、MDA(2.76μmol/L和1.99μmol/L)明显低于HI组(P<0.01),NO(44.16μmol/L和52.15μmol/L)、SOD(203.24 U/mL和237.86 U/mL)高于HI组(P<0.01)。光镜及透射电镜下观察HI组心肌结构破坏,心肌细胞呈灶状或片状坏死;线粒体损伤,核皱缩,核染色质边集。FDP组和预使用FDP组心肌细胞排列较有序,胞核线粒体稍肿胀。结论:果糖二磷酸钠可使氧自由基产生减少,增加NO含量,增强SOD活性,修复心肌缺氧缺血损伤。
AIM: To observe the effect and mechanism of fructose diphosphate (FDP) on myocardial injury induced by hypoxia-ischemia in neonatal rats. Methods: Forty newborn rats were randomly divided into 4 groups (10 in each group): sham operation group, HI group, FDP group and FDP group. The rats were sacrificed by ligation of coronary artery and hypoxia chamber Myocardial ischemia and hypoxia injury model. Serum levels of nitric oxide (NO), malondialdehyde (MDA), superoxide dismutase (SOD) and lactate dehydrogenase (LDH) were measured. The pathological changes of myocardium under light and transmission electron microscopy were observed. Results: Serum levels of LDH (7789.36 U / L) and MDA (4.30μmol / L) in HI group were significantly higher than those in sham operation group (3608.47 U / L, 1.76μmol / L) (P <0.01). The levels of serum LDH (4237.58 U / L and 3600.82 U / L) in FDP group and FDP group were significantly lower than those in sham operation group (115.49 U / mL vs 56.88μmol / L, ), MDA (2.76μmol / L and 1.99μmol / L) were significantly lower than those in HI group (44.16μmol / L and 52.15μmol / L), SOD (203.24 U / mL and 237.86 U / mL) Higher than HI group (P <0.01). Light microscope and transmission electron microscope were used to observe the damage of myocardial structure in HI group. The myocardial cells showed focal or lamellar necrosis; mitochondrial damage, nuclear shrinkage and nuclear chromatin margination. FDP group and pre-use of FDP group myocardial cells arranged more orderly, slightly swelling of the nuclear mitochondria. CONCLUSION: Sodium fructose diphosphate can reduce the generation of oxygen free radicals, increase the content of NO, enhance the activity of SOD and repair the myocardial injury caused by hypoxia and ischemia.