机构地区:[1]广州医学院第二附属医院麻醉科,广州510260 [2]中南大学湘雅二院麻醉科,长沙410011
出 处:《中华神经医学杂志》2009年第6期560-562,566,共4页Chinese Journal of Neuromedicine
摘 要:目的研究高张盐水对大鼠局灶性脑缺血再灌注损伤后脑含水量、肿瘤坏死因子-α(TNF-α)含量以及脑细胞凋亡的影响,探讨高张盐水在脑缺血再灌注损伤中的作用和机制。方法健康SD雄性大鼠96只按随机数字表法分为4组,即假手术组(P组)、单纯缺血再灌注组(IR组)、7.5%高张盐水组(HS—A组)、4.2%高张盐水组(HS-B组),每组各24只。采用线栓法制作大脑中动脉缺血模型,再灌注前经股静脉分别给予7.5%NaCl(HS-A组)或4.2%NaCl(HS-B组),P组和墩组不给任何药。检查再灌注前,再灌注后30min、60min、90min时的血清Na^+浓度。再灌注22h后,对大鼠进行神经功能缺陷评分,然后断头取脑检测左右两侧脑含水量;取缺血侧前脑皮质测TNF-α含量;取梗死灶周围脑组织,用TUNEL法检测神经元凋亡情况。结果输入高张盐水后,HS—A组和HS-B组大鼠血清Na^+浓度明显升高.HS—A组持续到再灌注后90min,HS-B组在再灌注60min后基本恢复正常。IR组大鼠两侧脑含水量较假手术组增加,缺血侧增加更明显,比较差异有统计学意义(P〈0.05)。HS—A组和HS—B组大鼠两侧脑含水量较IR组相比明显减少,并以缺血侧减少更明显,比较差异有统计学意义(P〈0.05);同IR组相比,HS—A组和HS—B组大鼠脑组织TNF-α含量明显降低,凋亡细胞计数明显下降,神经缺陷评分也明显下降,比较差异均有统计学意义(P〈0.05)。结论高张盐水可减少缺血再灌注后脑含水量和脑组织TNF-α含量,减轻脑细胞凋亡,改善缺血再灌注损伤后神经功能。Objective To investigate the effect ofhypertonic saline on cerebral water content, tumor necrosis factor-α (TNF-α) level and neuronal apoptosis following focal cerebral ischemia-reperfusion (IR) injury in rats and explore the mechanisms involved. Methods Ninety-six rats were randomized equally into 4 groups, namely the shame-operated group, untreated IR injury group, and 4.2% and 7.5% hypertonic saline groups (HS-A and HS-B groups, respectively). In the latter 3 groups, cerebral ischemia was induced by middle cerebral artery occlusion for 2 h followed by administration of the corresponding treatments. Serum sodium concentration was measured at 5 min before and at 30, 60 and 90 min after the reperfusion. At 22 h ofreperfusion, the rats were sacrificed after neurological deficit evaluation, and brain edema was assessed by measuring the wet-to-dry weight ratio of the brain tissue. TNF-α expression in the ischemic brain tissue was measured by enzyme-linked immunosorbent assay (ELISA), and the neuronal apoptosis was analyzed using TUNEL assay. Results In the saline-treated rats, serum sodium level increased significantly after saline administration, lasting for 60 min before recovering the normal levels in HS-A group and for over 90 min in HS-B group. Compared with that in the sham-operated group, the brain water content in rats of the IR group increased in both of the hemispheres, but more obviously in the ischemic hemisphere. In the two saline-treated groups, the water content decreased significantly in the bilateral hemispheres, which was especially obvious in the ischemic hemisphere; administration of 7.5% saline resulted in greater water content reduction in the ischemic hemisphere than 4.2% saline. Compared with the IR group, the two saline-treated groups showed significant reduction in TNF-α levels and apoptotic cells in the brain along with decreased neurological deficits. Conclusion Hypertonic saline can ameliorate cerebral focal IR injury by decreasing the cerebral water content, TNF-α l
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