二氧化硫对大鼠离体心脏功能影响的机制研究

为了探讨二氧化硫(SO2)对心脏功能影响的机制,分别用10、300和1000μmol·L-1的SO2灌流大鼠离体心脏后,测定心脏组织中一氧化氮(NO)、超氧化物歧化酶(SOD)、丙二醛(MDA)和谷胱甘肽(GSH)含量以及心脏灌流液中肌酸激酶(CK)和乳酸脱氢酶(LDH)活性.结果表明,10、300和1000μmol·L-1的SO2均可使心脏组织中NO和MDA含量以及心脏灌流液中CK和LDH活性明显增加,而使SOD和GSH含量明显减少.较高浓度(300和1000μmol·L-1)的SO2可使心脏组织中Na+K+-ATP酶和Ca2+Mg2+-ATP酶活性明显下降.结论:SO2对大鼠离体心脏功能影响的作用机制与SO2对心脏组织的氧化损伤作用、心肌细胞膜Na+K+-ATP酶和Ca2+Mg2+-ATP酶活性降低及NO-cGMP信号转导通路有关.

The mechanism of the effects of sulfur dioxide on heart function in isolated perfused rat heart

To investigate the mechanism of the effects of sulfur dioxide (SO2) on heart function, isolated rat hearts were perfused by 10, 300 and 1000 μmol·L-1 SO2, respectively. Then the contents of nitric oxide (NO), superoxide dismutase (SOD), reduced glutathione (GSH), malondialdehyde (MDA) in the hearts and the activities of lactate creatine kinase (CK) and dehydrogenase (LDH) in the perfusate were measured. The results showed that, at 10, 300 and 1000 μmol·L-1,SO2 significantly increased the contents of NO and MDA in the hearts and the activities of CK and LDH in the perfusate. But the contents of SOD and GSH in the hearts were significantly decreased. At high concentrations (300 and 1000 μmol·L-1), SO2 decreased the activities of Na+K+-ATPase and Ca2+Mg2+-ATPase in the hearts. These results suggested that the mechanism of the effects of SO2 on heart function might be related to the oxidative damage effect of SO2 on heart tissues, the decreased activities of Na+K+-ATPase and Ca2+Mg2+-ATPase, and the NO-cGMP signal transduction pathway.