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作 者:郭培培[1] 吴会生[2] 严虹[1] 陈璟莉[1] 袁世荧[3]
机构地区:[1]武汉市中心医院麻醉科,430014 [2]武汉大学中南医院麻醉科 [3]华中科技大学同济医学院附属协和医院麻醉科
出 处:《中华麻醉学杂志》2015年第3期377-379,共3页Chinese Journal of Anesthesiology
摘 要:目的评价右美托咪定对大鼠全脑缺血再灌注时氧化应激反应的影响。方法健康雄性SD大鼠36只,体重250—300g,采用随机数字表法分为3组(n=12):假手术组(S组)、全脑缺血再灌注组(I/R组)和右美托咪定组(D组)。采用夹闭双侧颈总动脉联合低血压法制备大鼠全脑缺血再灌注损伤模型。D组于再灌注即刻经颈总静脉注射右美托咪定3μg/kg负荷剂量,随后以3μg·kg^-1·h^-1的速率静脉输注至再灌注2h。于再灌注24h时行神经功能缺陷评分(NDS评分),然后处死大鼠,取脑组织,计数凋亡细胞,计算细胞凋亡率,测定丙二醛(MDA)、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的水平。结果与S组比较,I/R组和D组NDS评分、细胞凋亡率和MDA水平升高,SOD和CAT的水平降低(P〈0.01);与I/R组比较,D组NDS评分、细胞凋亡率和MDA水平降低,SOD和CAT的水平升高(P〈0.01)。结论右美托咪定通过抑制氧化应激反应减轻大鼠全脑缺血再灌注损伤。Objective To evaluate the effects of dexmedetomidine on the oxidative stress responses during global cerebral ischemia-reperfusion (I/R) in rats. Methods Thirty-six male Sprague-Dawley rats, weighing 250-300 g, were randomly divided into 3 groups (n= 12 each) using a random number table: sham operation group (group S), global cerebral I/R group (group I/R) and dexmedetomidine group (group D). Global cerebral ischemia was induced by occlusion of bilateral common carotid arteries com- bined with hypotension (MAP maintained at 35-45 mmHg). In group D, dexmedetomidine was infused at a rate of 3μg ·kg^-1 h^-1 until 2 h of reperfusion after a loading dose of dexmedetomidine 3μg/kg was intra- venously injected immediately after onset of reperfusion. The neurological deficit score (NDS) was assessed at 24 h of reperfusion, the rats were then sacrificed, and their brains were immediately removed for deter- mination of cell apoptosis and levels of malondialdehyde (MDA), superoxide dismutase (SOD) and cata- lase (CAT). Apoptotic rate was calculated. Results Compared with group S, NDS, apoptotic rate and MDA level were significantly increased, and SOD and CAT levels were decreased in I/R and D groups. Compared with group I/R, NDS, apoptotic rate and MDA level were significantly decreased, and SOD and CAT levels were increased in group D. Conclusion Dexmedetomidine attenuates global cerebral I/R injury through inhibiting the oxidative stress responses.
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