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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 order to investigate the changes of NO in brain tissue of rats with severe burns, 35% TBSA Ⅲ degree burn model was made in rats. The brain water content, NO 2 - / NO_3 ~ - and cyclic - guanosine monophosphate (cGMP) concentration, brain morphology was observed. The results showed that brain water content increased after burn, NO 2 - / NO 3 - and cGMP concentrations in brain tissue were higher than those in control group. Evans blue staining ranged widely, Nerve cells and cytoplasmic mitochondria swelling, increased intracellular blubber, capillary wall swelling, the basement membrane loose. Administration of NO synthase (NOS) inhibitor monomethylarginine (L-NMMA) significantly reduced NO 2 - / NO 3 - and brain water content. Prompted NOS activity in the brain tissue after burn caused NO excessive production is caused by increased cerebral vascular permeability, brain ischemia, hypoxia and cerebral edema one of the reasons.