高碳酸血癥對(duì)嚴(yán)重低氧缺血大鼠腦損傷的影響
發(fā)布時(shí)間：2018-11-03 17:51
【摘要】：目的研究高碳酸血癥對(duì)嚴(yán)重低氧缺血大鼠腦損傷的影響及其機(jī)制。方法雄性SD大鼠48只,隨機(jī)分為假手術(shù)組(S組)、低氧缺血組(HI組)和高碳酸血癥組(HP組),每組16只。S組暴露左側(cè)頸總動(dòng)脈但不結(jié)扎,1h后機(jī)械通氣,維持PaO_2和PaCO_2在正常水平3h。制作低氧缺血模型,HI組吸入11%~13%O_2并維持PaO_230~49mm Hg;HP組在HI組的基礎(chǔ)上吸入11%~13%O_2-8%CO_2-N2混合氣維持PaO_230~49mm Hg,PaCO_260~80mm Hg。機(jī)械通氣3h后處死大鼠,觀察腦組織水腫及病理改變,采用TUNEL法檢測(cè)皮質(zhì)神經(jīng)元凋亡,應(yīng)用FITC-dextran檢測(cè)血腦屏障通透性的變化,免疫熒光法檢測(cè)皮質(zhì)水通道蛋白4(AQP4)及缺血區(qū)皮質(zhì)內(nèi)皮細(xì)胞的標(biāo)記物(RECA-1)的表達(dá),Western blot法檢測(cè)AQP4的蛋白含量變化。結(jié)果與S組比較,HI組和HP組血腦屏障通透性明顯升高,腦含水量明顯增加(P0.05);與HI組比較,HP組腦含水量明顯增加(P0.05),腦組織損傷加重,TUNEL染色陽性細(xì)胞數(shù)明顯增加(P0.05),腦皮質(zhì)AQP4蛋白含量明顯升高,RECA-1熒光強(qiáng)度明顯降低,斷離現(xiàn)象明顯增多,血腦屏障通透性明顯增加(P0.05)。結(jié)論高碳酸血癥加重了嚴(yán)重的低氧缺血性腦損傷,其機(jī)制可能與腦皮質(zhì)AQP4蛋白表達(dá)的增加和血腦屏障的破壞有關(guān)。
[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.
【作者單位】： 哈爾濱醫(yī)科大學(xué)附屬第二醫(yī)院麻醉科;中山大學(xué)附屬第六醫(yī)院麻醉科;
【基金】：國家自然科學(xué)基金(81171076,81400989) 黑龍江省青年科學(xué)基金項(xiàng)目(QC2011C004)
【分類號(hào)】：R741
本文編號(hào)：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.
【作者單位】： 哈爾濱醫(yī)科大學(xué)附屬第二醫(yī)院麻醉科;中山大學(xué)附屬第六醫(yī)院麻醉科;
【基金】：國家自然科學(xué)基金(81171076,81400989) 黑龍江省青年科學(xué)基金項(xiàng)目(QC2011C004)
【分類號(hào)】：R741
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1 吳樹彬;劉晉萍;;高碳酸血癥腦保護(hù)作用的研究進(jìn)展[J];中國體外循環(huán)雜志;2013年02期
，本文編號(hào)：2308514
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