氨基胍干预对第三腰椎横突综合征模型大鼠骨骼肌诱导型一氧化氮合酶及一氧化氮的影响*

背景：研究表明，诱导型一氧化氮合酶及一氧化氮在急性软组织损伤及其修复过程中起到重要的作用，但目前有关其在慢性软组织损伤修复过程中的作用，及氨基胍对其作用的影响尚不明确。目的：探讨慢性软组织损伤模型——第三腰椎横突综合征模型大鼠损伤局部软组织诱导型一氧化氮合酶活性及一氧化氮含量与炎症反应及软组织损伤程度的关系，并观察氨基胍干预后对以上关系的影响。设计、时间及地点：随机对照动物实验，于2007-09/2008-09在解放军海军总医院海战伤研究中心二级实验室完成。材料：将96只SD大鼠抽签法随机分为正常组、模型组及氨基胍组共3组，每组32只。方法：模型组将0.3 cm×0.3 cm大小的明胶海绵置入第三腰椎横突后半段深筋膜中层下制备第三腰椎横突综合征动物模型；氨基胍组从造模14 d开始，按50 mg/kg剂量经腹膜内给药，2次/d，直至处死前1 d为止；正常组为不做任何干预。主要观察指标：于首次氨基胍干预后1，3，7，14 d检测各组第三腰椎横突周围骨骼肌及其他软组织诱导型一氧化氮合酶免疫组织化学灰度值、一氧化氮含量及观察组织形态学变化。结果：模型组损伤局部软组织诱导型一氧化氮合酶活性及一氧化氮含量比正常组明显升高(P < 0.01)，且与损伤局部炎症反应及组织损伤程度相一致。氨基胍组诱导型一氧化氮合酶活性及一氧化氮含量比模型组明显降低(P < 0.01)，损伤局部炎症反应及组织损伤程度明显减轻。结论：第三腰椎横突综合征动物模型中由炎性因子诱导诱导型一氧化氮合酶大量表达生成的高浓度的一氧化氮是造成慢性软组织损伤的重要因素。而这种作用可以被氨基胍所抑制，为慢性软组织损伤的修复创造了有利条件。

Effect of aminoguanidine intervention on inducible nitric oxide synthase and NO in the skeletal muscles of rats with third lumbar processus transverses syndrome

BACKGROUND: Previous studies demonstrate that inducible nitric oxide synthase (iNOS) and NO play important roles in both the occurrence and the recovery of acute soft tissue injury; however, their effect on the recovery of chronic injury, especially, the influence of aminoguanidine (AG) on recovery of acute soft tissue injury remains unclear. OBJECTIVE: To study the relation between the iNOS activity and NO content in the skeletal muscles and the injury condition of soft tissue and inflammatory reaction in rats with third lumbar processus transverses vertebrarum syndrome, in addition, to observe the treatment effectives of AG intervention. DESIGN, TIME AND SETTING: A randomized controlled animal experiment was performed at the Second Class War Injury Laboratory, Naval General Hospital of Chinese PLA between September 2007 and September 2008.MATERIALS: Ninety-six SD rats were randomly divided into normal, model, and AG groups, with 32 rats in each group. METHODS: Rats in the model group were created third lumbar processus transverses vertebrarum syndrome models by inserting 0.3 cm×0.3 cm gelatin sponge in the back part of the deep fascia of third lumbar vertebra. Animals in the AG group were intra-peritoneum administrated 50 mg/kg AG, twice a day from the 14th day after the model preparation to the day before execution. No intervention was given to the normal group.MAIN OUTCOME MEASURES: iNOS expression, NO content and histomorphological changes of the soft tissues in the third lumbar vertebra were observed at the days 1, 3, 7 and 14 after AG intervention.RESULTS: iNos activity and NO content in the model group was significantly higher than the normal group (P < 0.01), the inflammatory reaction was in competence with the condition of soft tissue injuries. iNos activity and NO content in the AG group were significantly lower than the model group (P < 0.01), and the inflammatory reaction and injury condition in the injured soft tissue was significantly released.CONCLUSION: The high level of iNOS, induced by the inflammatory factors in the third lumbar processus transverses vertebrarum syndrome model rats, can lead to high content of NO, which is an important impact factor contributes to the chronic soft tissue injury. This course can be restrained by AG. Therefore, AG created favorable conditions for the recovery of chronic soft tissue injury.