亚低温对继发性脑损伤保护作用的研究进展(2)
作者:佚名; 更新时间:2014-12-13
,脂质过氧化反应产物丙二醛含量明显增高,自由基清除剂超氧化物歧化酶(SOD)活性明显下降,神经元核膜、线粒体、内质网等结构严重受损. MHT降低花生四烯酸的代谢率,并可能抑制自由基、烷基及其他生物活性代谢物产生. MHT还使脑脊液和脑组织丙二醛含量明显下降,SOD活性明显升高,神经元超微结构损害明显减轻.

    4.8抑制一氧化氮合酶(iNos)的活性,减少一氧化氮(No)的合成NO可以自由穿过细胞膜,参与机体许多生理和病理过程. 一般认为诱生型iNOS激活产生的大量NO与脑损伤有关,而内皮型NOS(eNOS)激活产生的NO是维持脑血流量的重要因素. NO和氧自由基(O2-)反应产生的过氧化亚硝基阴离子及其降解产物均具有强大毒性. 缺血后正常体温组亚硝酸盐浓度明显升高,cGMP水平升高了3倍,NOS活性显著升高,而MHT组则无这些变化. Kumur等[18]也通过实验证实了MHT能抑制脑缺血再灌注引起的颈静脉内NO升高.

    4.9其他可能的机制有的学者从另外的角度来解释亚低温的作用机制,如受损后脑组织的炎症反应程度作为评价亚低温疗效的指标. 亚低温可以通过有效地抑制某些细胞因子介导的脑组织炎 症反应达到脑创伤后的治疗效果. 国外学者Chatzipanteli等[19]发现亚低温能抑制炎症反应过程.

    5亚低温治疗脑损伤的展望

    现有的实验结果表明,无论动物实验和临床实践都证明30℃~35℃的亚低温具有肯定的脑保护疗效. 但从临床应用的方面,我们还应进一步深入探讨亚低温的最佳适应证、时间窗、温度窗及亚低温实施方法等问题;虽然我们还不清楚其具体的保护机制,但可以预见的是,随着医学、细胞及分子生物学的飞速发展,我们在不久的将来会研究发现亚低温脑保护的机制,并将其有效地应用于临床实践.

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