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急性CO中毒大鼠脑内VCAM-1表达CD4+T淋巴细胞浸润规律的研究及高压氧干预后的变化
引用本文:吕晓宁,李金声,常耀明,张然,王文岚,谢小平.急性CO中毒大鼠脑内VCAM-1表达CD4+T淋巴细胞浸润规律的研究及高压氧干预后的变化[J].中国急救医学,2007,27(3):225-228,289.
作者姓名:吕晓宁  李金声  常耀明  张然  王文岚  谢小平
作者单位:710032,西安,解放军第四军医大学航空航天医学系航空卫生与卫生勤务学教研室
摘    要:目的 观察急性CO中毒后大鼠脑内血管内皮细胞黏附分子-1(VCAM-1)表达、CD4^+T淋巴细胞浸润情况,从系统细胞免疫反应角度探讨迟发性脑病(DNS)与免疫反应的关系。方法 30只SD雄性大鼠随机分为对照组,染毒后1、3、7d组和高压氧(HBO)治疗7d组,每组6只。采用HE和免疫组织化学染色方法,观察染毒后各时间点大鼠脑内病理形态学变化,及VCAM-1表达、CD4^+T淋巴细胞浸润情况。结果 对照组无VCAM-1表达、无CD4^+T淋巴细胞浸润;各染毒组大鼠脑内微血管内皮细胞和变性坏死的神经元均有VCAM-1不同程度的表达。染毒后1d组为表达高峰(P〈0.01),3d组VCAM-1的表达数量有所减少。此时,局部大脑皮层开始有CD4^+T淋巴细胞浸润;至染毒后7d,在部分变性坏死的神经元上仍有VCAM-1的持续表达,而CD4^+T淋巴细胞浸润达高峰(P〈0.01)。染毒后立即进行HBO治疗7d,其VCAM-1、CD4^+T淋巴细胞均显著减少,与染毒后7d组相比差异有统计学意义(P〈0.05)。结论 系统细胞免疫反应可能参与了DNS的发生。

关 键 词:急性CO中毒  血管内皮细胞黏附分子-1  CD4  T淋巴细胞  迟发性脑病  高压氧
文章编号:1002-1949(2007)03-0225-04
修稿时间:2006-11-07

Expression of VCAM-1 and Infiltration of CD4+ T lymphocytes in brains of acute CO-poisoning rats and development after treated by HBO
LV Xiao - ning , LI Jin - sheng , CHANG Yao - ruing,et al..Expression of VCAM-1 and Infiltration of CD4+ T lymphocytes in brains of acute CO-poisoning rats and development after treated by HBO[J].Chinese Journal of Critical Care Medicine,2007,27(3):225-228,289.
Authors:LV Xiao - ning  LI Jin - sheng  CHANG Yao - ruing  
Institution:LV Xiao - ning , LI Jin - sheng , CHANG Yao - ruing, et al.
Abstract:Objective To investigate the expression of Vascular Cell Adhesion Molecule-1 (VCAM-1) and the infiltration of CD4 T lymphocytes in brains of acute Carbon Monoxide (CO) poisoned rats and study the relation of Delayed Neuropathological Sequelae (DNS) and immunoreaction through systemic cell immunoreaction . Methods CO-poisoned rats model was established in Twenty-four SD male rats and another six as control. The poisoned rats were equally divided into four groups: 1, 3,7 d post-poisoning and 7 d post-Hyperbaric Oxygen(HBO) treatment respectively. HE and Immunohistochemical staining were performed on frozen sections to observe the change of pathological morphous and the expression of VCAM-1 and the infiltration of CD4 T lymphocytes in brains of each group rats as compared with that of the control rats. Rrsults Immunohistochemical staining showed that there were expressions of VCAM-1 in endothelial cells of cerebral microvessels and denaturatd neurons in poisoned group rats at a disparate degree, but no VCAM-1 expression and CD4 T lymphocytes infiltration were shown in control rats. VCAM-1 expression reached the peak at 1th d(P<0.01) and became weak at 3th d and kept at 7th d, while CD4 T lymphocytes initiated infiltration in poisoned rats partial cerebral cortex at 3th d and reached the peak at 7th d(P<0.01). Moreover, the results of VCAM-1 expression and CD4 T lymphocytes decreased greatly at HBO group and they both possessed significant statistical difference (P<0.05) respectively compared with that of 7th d post-poisoning. Conclusions Systemic cell immunoreaction was contributed to DNS possibly.
Keywords:Acute CO poisoning  Vascular cell adhesion molecule-1  CD4  lymphocytes  Delayed neuropathological sequelae  Hyperbaric oxygen
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