放射损伤、烧伤及放烧复合伤大鼠早期心肌一氧化氮的变化及其对心肌的作用

Changes of nitric oxide production and its effects on myocardium at the early stage after radiation, burn and combined radiation-burn injuries in rats

目的：研究６Ｇｙ放射损伤（Ｒ）、烧伤（Ｂ）及放烧复合伤（ＲＢ）早期心肌一氧化氮（ＮＯ）合成的变化及其对心肌的作用。方法：观测三种损伤大鼠伤后２４ｈ心肌ＮＯ含量、一氧化氮合酶（ＮＯＳ）活性的变化，ＮＯ供体ＳＩＮ－１对正常大鼠心肌ｃＧＭＰ、Ｎａ＋－Ｋ＋－ＡＴＰ酶活性的影响。结果：Ｂ组和ＲＢ组心肌ＮＯ的合成及诱生型ＮＯＳ活性明显增强，Ｒ组无变化（Ｐ＞０．０５）。ＮＯ供体ＳＩＮ－１致心肌ｃＧＭＰ合成增加及心肌膜Ｎａ＋－Ｋ＋－ＡＴＰ酶活性下降，地塞米松对以上变化有明显抑制作用。结论：Ｂ和Ｒ组早期心肌ＮＯ合成增强，主要起因于诱生型ＮＯＳ的过量表达，进一步引起心肌ｃＧＭＰ含量和Ｎａ＋－Ｋ－＋ＡＴＰ酶活性的改变。

Objective: To observe the changes of nitric oxide (NO) production in and its effects on myocardium at the early stage after radiation, burn and combined radiation burn injuries. Methods: 1) The myocardial NO content during the first 24 hours and the activity of nitric oxide synthase (NOS) at the 8th hour after injuries were determined; 2) cGMP level and Na + K + ATPase activity were assessed in the myocardium treated with NO donor SIN 1 in normal animals and that with dexamethasone in those with combined radiation burn injury. Results: There was a significant increase in NO production and NOS activity in the myocardium with a peak at the 8th hour after burn and combined radiation burn injuries. No obvious alteration was seen in the animals with radiation injury. Treatment with NO donor Sin 1 caused a marked elevation in cGMP level and an obvious decline in membrane Na + K + ATPase activity in the myocardium. However, treatment of the animals with combined radiation burn injury using dexamethasone did inhibit the increase in cGMP level and decrease in Na + K + ATPase activity. Conclusion: Overproduction of NO, probably caused by excessive expression of iNOS in the myocardium after burn and combined radiation burn injuries, might be involved in the modulation of cGMP production and Na + K + ATPase activity in the myocardium.