摘要
目的:了解创伤性脑损伤(TBI)后血浆中一氧化氮(NO)含量、一氧化氮合酶(NOS)活性及与脑水肿间关系。方法:36只SD大鼠,随机分为6组:对照组6只、按动物处死6、24、72、120、168h不同时间分为5组,每组6只。上述各组用硝酸还原酶法测定血清中NO、NOS含量,及测定脑组织含水量。结果:(1)TBI后血浆内NO含量、NOS活力即有升高,在伤后6h即有升高,72h明显升高并一直处于较高水平,与对照组比较差异有统计学意义(P<0.05)。(2)脑组织含水量在外伤后升高,与对照组比较差异有统计学意义(P<0.05)。与血浆中NO含量、NOS活力变化趋势一致。结论:大鼠创伤性脑损伤后NO、NOS的升高与脑水肿发生有关。提示临床处理脑损伤时早期补充外源性NOS清除剂,与脱水剂联合使用,可减轻脑水肿继发性损伤。
Objective :To determine and evaluate the changes of NO and NOS in serum after traumatic brain injury and relationship between them and brain edema, and at the same time to detect the changes of NO and NOS in serum and the relationship between these changes and positive NOS neurons. Method:thirty-six SD rats were used and divided into two groups: the normal control and the operation group. The cerebral contusion model was produced by dropping weight. The traumatic brain injury model was built successfully and contents of NO and NOS in cerebral contusion tissue were measured, so were brain water contents and changes of NO and NOS in serum. Results: (1)Data of the normal control and the operation groups were significantly different (P〈0.05).(2) NO values of the traumatic fight hemisphere were significantly higher than those of the normal control group, so were brain water contents and NO in serum (P〈0.05).NOS activity of the traumatic hemisphere was higher than that of the operation group (P〈0.05),so was in serum. Conclusions:The results of this study suggests that No and NOS in rats after the injury increase, which is related to the occurrence of cerebral edema, by prompt early clinical treatment of brain injury with addition of exogenous NOS scavenger, in conjunction with dehydrating agents, it is possible to reduce brain edema in secondary injury.
出处
《交通医学》
2012年第3期213-216,共4页
Medical Journal of Communications