右美托咪定后处理对大鼠脑缺血再灌注损伤组织的保护作用
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摘要
目的:探讨不同浓度右美托咪定后处理对大鼠脑缺血再灌注损伤组织的作用。方法:72只Wistar大鼠分为4组,每组18只。假手术组仅暴露颈外动脉;缺血再灌注组(I/R组)于脑缺血60 min后再灌注,并由腹腔注射无菌生理盐水1 m L;右美托咪定Ⅰ组和Ⅱ组于脑缺血60 min后再灌注,然后分别由腹腔注射50和100μg/g右美托咪定。再灌注后第1、3、7天,对大鼠神经功能进行评分,取脑组织,HE染色,光镜下观察缺血侧核心区域以及半影区域的组织形态。计算再灌注第3天脑梗死面积/全脑面积比值。结果:再灌注后第1、3、7天,与假手术组比较,I/R组神经功能评分降低;与I/R组比较,右美托咪定Ⅰ、Ⅱ组神经功能评分升高(P <0. 05)。再灌注后第1、3、7天,大脑皮层HE染色显示右美托咪定Ⅰ、Ⅱ组的半影区较I/R组神经细胞层次清晰,细胞数量增加且形状较为完整,同时间质水肿减轻。再灌注后第3天,右美托咪定Ⅰ、Ⅱ组大鼠脑梗死面积/全脑面积比值低于I/R组(P <0. 05)。结论:右美托咪定后处理对大鼠脑缺血再灌注损伤组织具有一定的保护作用。
Aim: To investigate the effects of dexmedetomidine postconditioning on cerebral tissue after ischemia-reperfusion injury in rats. Methods: A total of 72 Wistar rats were allocated into 4 groups(n = 18),the sham operation group only exposed the external carotid artery,the ischemia-reperfusion group(I/R group) was given 1 m L normal saline by intraperitoneal injection after cerebral ischemia for 60 min and reperfusion,and dexmedetomidine group Ⅰ and group Ⅱ were administered 50 and 100 μg/kg dexmedetomidine by intraperitoneal injection after cerebral ischemia for 60 min and reperfusion,respectively. On the 1 st,3 rd,and 7 th day after reperfusion,the neurologic status of the rats was evaluated,then the brain tissue was stained with HE staining,and the tissue morphology of the core area of the ischemic side and the penumbra region was observed under the optical microscope. The ratio of cerebral infarction area to total brain area was calculated on the 3 rd day after reperfusion. Result: On the 1 st,3 rd and 7 th day after reperfusion,the neurological function scores of the I/R group decreased compared with the sham operation group,which increased in the dexmedetomidine group Ⅰ and Ⅱcompared with the I/R group(P < 0. 05). HE staining of cerebral cortex showed that the penumbra region of the dexmedetomidine group Ⅰ and Ⅱ had clearer layers of nerve cells than that of the I/R group. The number and shape of nerve cells both improved and the interstitial edema alleviated. On the 3 rd day after reperfusion,the ratio of cerebral infarction area to total brain area in the dexmedetomidine group Ⅰ and Ⅱ was lower than that in the I/R group(P < 0. 05). Conclusion: Dexmedetomidine postconditioning has protective effects on rat cerebral tissue after ischemia-reperfusion injury.
Aim: To investigate the effects of dexmedetomidine postconditioning on cerebral tissue after ischemia-reperfusion injury in rats. Methods: A total of 72 Wistar rats were allocated into 4 groups(n = 18),the sham operation group only exposed the external carotid artery,the ischemia-reperfusion group(I/R group) was given 1 m L normal saline by intraperitoneal injection after cerebral ischemia for 60 min and reperfusion,and dexmedetomidine group Ⅰ and group Ⅱ were administered 50 and 100 μg/kg dexmedetomidine by intraperitoneal injection after cerebral ischemia for 60 min and reperfusion,respectively. On the 1 st,3 rd,and 7 th day after reperfusion,the neurologic status of the rats was evaluated,then the brain tissue was stained with HE staining,and the tissue morphology of the core area of the ischemic side and the penumbra region was observed under the optical microscope. The ratio of cerebral infarction area to total brain area was calculated on the 3 rd day after reperfusion. Result: On the 1 st,3 rd and 7 th day after reperfusion,the neurological function scores of the I/R group decreased compared with the sham operation group,which increased in the dexmedetomidine group Ⅰ and Ⅱcompared with the I/R group(P < 0. 05). HE staining of cerebral cortex showed that the penumbra region of the dexmedetomidine group Ⅰ and Ⅱ had clearer layers of nerve cells than that of the I/R group. The number and shape of nerve cells both improved and the interstitial edema alleviated. On the 3 rd day after reperfusion,the ratio of cerebral infarction area to total brain area in the dexmedetomidine group Ⅰ and Ⅱ was lower than that in the I/R group(P < 0. 05). Conclusion: Dexmedetomidine postconditioning has protective effects on rat cerebral tissue after ischemia-reperfusion injury.
引文
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[15]NAKANO T,OKAMOTO H.Dexmedetomidine-induced cerebral hypoperfusion exacerbates ischemic brain injury in rats[J].J Anesth,2009,23(3):378
[2]赵京禹,费翔,郭徽,等.右美托咪定预处理对小鼠肠缺血再灌注损伤的作用研究[J].现代生物医学进展,2014,14(35):6823
[3]秦汉,程江霞,赵彬,等.右美托咪定联合浅低温处理对大鼠脑缺血术后认知功能的影响[J].华中科技大学学报(医学版),2014,43(1):76
[4]贾建丽,蔡劲松,戚翔,等.右美托咪定预先给药对大鼠全脑缺血再灌注损伤的影响[J].河北医药,2015,37(17):2565
[5]ZAUSINGER S,HUNGERHUBER E,BAETHMANN A,et al.Neurological impairment in rats after transient middle cerebral artery occlusion:a comparative study under various treatment paradigms[J].Brain Res,2000,863(1/2):94
[6]JI Y,YAN X,HU Y,et al.Dh HP-6 attenuates cerebral ischemia-reperfusion injury in rats through the inhibition of apoptosis[J].Mol Med Rep,2017,16(5):7229
[7]SOLTYS Z,JANECZKO K,ORZYOWSKA-SLIWINSKAO,et al.Morphological transformations of cells immunopositive for GFAP,Trk A or p75 in the CA1 hippocampal area following transient global ischemia in the rat.A quantitative study[J].Brain Res,2003,987(2):186
[8]董海平,周薇,王震虹,等.右美托咪定预处理经AMPK/SIRT1通路抑制大鼠脑缺血再灌注损伤的炎性反应[J].中国医药导报,2018,15(1):4
[9]刘付宁,纪风涛,何惠燕,等.右美托咪定对大鼠脑缺血再灌注损伤后星形胶质细胞的影响[J].中国病理生理杂志,2012,28(10):1751
[10]YALCIN S,AYDOGAN H,KUCUK A.Supplemental oxygen in elective cesarean section under spinal anesthesia:handle the sword with care[J].Braz J Anesthesiol,2013,63(5):393
[11]ZHOU HY,ZHANG LN,ZHENG MZ,et al.Improved myocardial function with supplement of levosimendan to Celsior solution[J].J Cardiocasc Pharmacol,2014,64(3):256
[12]KONISHI T.Brain oxidative stress as basic target of antioxidant traditional oriental medicines[J].Nerochem Res,2009,34(4):711
[13]FISHER M,FEUERSTEIN G,HOWELLS DW,et al.Update of the stroke therapy academic industry roundtable preclinical recommendations[J].Stroke,2009,40(6):2244
[14]SHIMIZU M,SEXENA P,KONSTANTINOV IE,et al.Remote ischemic preconditioning decreases adhesion and selectively modifies functional responses of human neutrophils[J].J Surg Res,2010,158(1):155
[15]NAKANO T,OKAMOTO H.Dexmedetomidine-induced cerebral hypoperfusion exacerbates ischemic brain injury in rats[J].J Anesth,2009,23(3):378