高碳酸血症对严重低氧缺血大鼠脑损伤的影响
发布时间：2018-11-03 17:51
【摘要】：目的研究高碳酸血症对严重低氧缺血大鼠脑损伤的影响及其机制。方法雄性SD大鼠48只,随机分为假手术组(S组)、低氧缺血组(HI组)和高碳酸血症组(HP组),每组16只。S组暴露左侧颈总动脉但不结扎,1h后机械通气,维持PaO_2和PaCO_2在正常水平3h。制作低氧缺血模型,HI组吸入11%~13%O_2并维持PaO_230~49mm Hg;HP组在HI组的基础上吸入11%~13%O_2-8%CO_2-N2混合气维持PaO_230~49mm Hg,PaCO_260~80mm Hg。机械通气3h后处死大鼠,观察脑组织水肿及病理改变,采用TUNEL法检测皮质神经元凋亡,应用FITC-dextran检测血脑屏障通透性的变化,免疫荧光法检测皮质水通道蛋白4(AQP4)及缺血区皮质内皮细胞的标记物(RECA-1)的表达,Western blot法检测AQP4的蛋白含量变化。结果与S组比较,HI组和HP组血脑屏障通透性明显升高,脑含水量明显增加(P0.05);与HI组比较,HP组脑含水量明显增加(P0.05),脑组织损伤加重,TUNEL染色阳性细胞数明显增加(P0.05),脑皮质AQP4蛋白含量明显升高,RECA-1荧光强度明显降低,断离现象明显增多,血脑屏障通透性明显增加(P0.05)。结论高碳酸血症加重了严重的低氧缺血性脑损伤,其机制可能与脑皮质AQP4蛋白表达的增加和血脑屏障的破坏有关。
[Abstract]:Objective to study the effect and mechanism of hypercapnia on brain injury in rats with severe hypoxic ischemia. Methods Forty-eight male SD rats were randomly divided into three groups: sham operation group (S group), hypoxic ischemia group (HI group) and hypercapnia group (HP group). PaO_2 and PaCO_2 were maintained at normal level for 3 h. Model of hypoxic ischemia, HI group inhaled 11%~13%O_2 and PaO_230~49mm Hg;HP group inhaled 11%~13%O_2-8%CO_2-N2 mixture to maintain PaO_230~49mm Hg,PaCO_260~80mm Hg. on the basis of HI group Three hours after mechanical ventilation, the rats were killed to observe the brain edema and pathological changes, the apoptosis of cortical neurons was detected by TUNEL method, and the permeability of blood-brain barrier was detected by FITC-dextran. The expression of cortical aquaporin 4 (AQP4) and cortical endothelial cell marker (RECA-1) were detected by immunofluorescence. The protein content of AQP4 was detected by, Western blot method. Results compared with group S, the blood brain barrier permeability and brain water content in HI and HP groups were significantly increased (P0.05). Compared with HI group, brain water content in HP group was significantly increased (P0.05), brain tissue injury was aggravated, the number of positive cells for TUNEL staining was significantly increased (P0.05), the content of AQP4 protein in cerebral cortex was significantly increased, and the fluorescence intensity of RECA-1 was significantly decreased. Breaking phenomenon increased significantly, blood-brain barrier permeability increased significantly (P0.05). Conclusion hypercapnia exacerbates severe hypoxic ischemic brain damage, and its mechanism may be related to the increase of AQP4 protein expression and the breakdown of blood-brain barrier.
【作者单位】： 哈尔滨医科大学附属第二医院麻醉科;中山大学附属第六医院麻醉科;
【基金】：国家自然科学基金(81171076,81400989) 黑龙江省青年科学基金项目(QC2011C004)
【分类号】：R741
本文编号：2308514
[Abstract]:Objective to study the effect and mechanism of hypercapnia on brain injury in rats with severe hypoxic ischemia. Methods Forty-eight male SD rats were randomly divided into three groups: sham operation group (S group), hypoxic ischemia group (HI group) and hypercapnia group (HP group). PaO_2 and PaCO_2 were maintained at normal level for 3 h. Model of hypoxic ischemia, HI group inhaled 11%~13%O_2 and PaO_230~49mm Hg;HP group inhaled 11%~13%O_2-8%CO_2-N2 mixture to maintain PaO_230~49mm Hg,PaCO_260~80mm Hg. on the basis of HI group Three hours after mechanical ventilation, the rats were killed to observe the brain edema and pathological changes, the apoptosis of cortical neurons was detected by TUNEL method, and the permeability of blood-brain barrier was detected by FITC-dextran. The expression of cortical aquaporin 4 (AQP4) and cortical endothelial cell marker (RECA-1) were detected by immunofluorescence. The protein content of AQP4 was detected by, Western blot method. Results compared with group S, the blood brain barrier permeability and brain water content in HI and HP groups were significantly increased (P0.05). Compared with HI group, brain water content in HP group was significantly increased (P0.05), brain tissue injury was aggravated, the number of positive cells for TUNEL staining was significantly increased (P0.05), the content of AQP4 protein in cerebral cortex was significantly increased, and the fluorescence intensity of RECA-1 was significantly decreased. Breaking phenomenon increased significantly, blood-brain barrier permeability increased significantly (P0.05). Conclusion hypercapnia exacerbates severe hypoxic ischemic brain damage, and its mechanism may be related to the increase of AQP4 protein expression and the breakdown of blood-brain barrier.
【作者单位】： 哈尔滨医科大学附属第二医院麻醉科;中山大学附属第六医院麻醉科;
【基金】：国家自然科学基金(81171076,81400989) 黑龙江省青年科学基金项目(QC2011C004)
【分类号】：R741
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1 吴树彬;刘晋萍;;高碳酸血症脑保护作用的研究进展[J];中国体外循环杂志;2013年02期
，本文编号：2308514
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