摘要
为探讨严重烧伤大鼠脑组织NO的变化,实验制作大鼠35%TBSAⅢ度烧伤模型,于伤后2、6、12、24 h测定了大鼠脑水含量、脑组织NO代谢产物NO_2^-/NO_3^-和环—磷酸鸟苷(cGMP)浓度,进行了脑形态学观察。结果显示:烧伤后脑水含量升高、脑组织NO_2^-/NO_3^-和cGMP浓度高于对照组;伊文思蓝蓝染范围广、染色深;脑内ATP酶减少;电镜观察血管内皮细胞、神经细胞及胞浆内线粒体肿胀,胞饮泡增多,毛细血管壁肿胀、基底膜疏松。给予NO合成酶(NOS)抑制剂单甲基精氨酸(L—NMMA),可使NO_2^-/NO_3^-和脑水含量明显降低。提示烧伤后脑组织内NOS活性升高导致NO产生过多,是造成脑血管通透性增加、脑组织缺血、缺氧及脑水肿的原因之一。
In this experiment we studied the effects of thermal injury on the production ot nitric oxide (NO) in rat brain tissues and the changes of brain in water content and morphology. We measured the levels of NO_2^-/NO_3^- (the stable end—products of NO), cGMP and the brain water content at the points of 2,6,12 and 24 hours after burn injury (35% TBSA full—thickness). The results showed that the levels of NO_2^-/NO_3^- and cGMP as well as the brain water content were increased. Evans blue discoloration of the rat brain in the experimental groups was much higher than that in the control group. ATPase was decreased in the experimental groups. The electronmicroscopy showed that the capillary endothelial cells, the neuron and their mitochodrid swelled. The pinocytotic resicle was increased. The capillary walls were swollen. After giving L-NMMA, a specific inhibitor of synthetase (NOS),the levels of NO_2^-/NO_3^- and the brain water content were significantly decreased. The experimental study suggested that increment in NO induced by high NOS activity in brain tissues may be one of causative factors of increase of brain vascular permeability, hypoxia, ischemia and edema of brain tissues after burn injury.
出处
《武警医学》
CAS
1997年第6期311-314,共4页
Medical Journal of the Chinese People's Armed Police Force
