Effects of Dexmedetomidine on Microregional O2 Balance during Reperfusion after Focal Cerebral Ischemia

Effects of Dexmedetomidine on Microregional O2 Balance during Reperfusion after Focal Cerebral Ischemia
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DOI:
10.1016/j.jstrokecerebrovasdis.2014.08.004
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发表时间:
2015-01-01
影响因子:
2.5
通讯作者:
Weiss, Harvey R.
Weiss, Harvey R.
中科院分区:
医学4区
文献类型:
--
作者:
Chi, Oak Z.;Grayson, Jeremy;Weiss, Harvey R.

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背景:应用α(2)-肾上腺素受体激动剂和镇静剂右美托咪定治疗脑缺血再灌流是否存在微区O-2平衡与神经元存活之间的关系。方法:大鼠大脑中动脉闭塞1h,再灌注2 h。再灌注期给予生理盐水(n=14)或右美托咪定1mg/kg/min(n=14)静脉滴注。再灌流2小时后,用~(14)I-安替比林放射自显影测定局部脑血流量,用冷冻分光光度法测定微区动脉和静脉(直径20~60 mm)氧饱和度(SvO(2)),并测定皮质梗塞面积。结果:缺血再灌注使微区SVO(2)降低(52.9+/-3.7%比61.1+/-.6%,P&lt;.005),变异或异质性增加(P&lt;.0001),但局部脑血流量和氧耗量相似。右美托咪定在再灌注期降低了SVO(2)的异质性,经方差分析(P&lt;.01),报告的变异系数(100 x标准差/均值)(11.8比16.4)。右美托咪定治疗后血氧饱和度<50%的静脉数目减少(13/80比27/81,P<0.01)。皮质梗塞占总皮质的百分比较小(8.3+/-2.2%vs.12.6+/-1.5%,P&lt;.005)。结论:在脑缺血再灌流皮质,右美托咪定减少了SVO(2)的异质性,减少了低氧饱和度的小静脉数量,改善了微区性氧供/耗平衡。改善伴随着皮质梗塞面积的缩小。
Background: This study was performed to determine whether there is an association between microregional O-2 balance and neuronal survival in cerebral ischemia-reperfusion using dexmedetomidine, an alpha(2)-adrenoreceptor agonist and a sedative. Methods: Rats were subjected to 1 hour middle cerebral artery occlusion and a 2-hour reperfusion. During reperfusion, normal saline (n = 14) or dexmedetomidine 1 mu g/kg/minute (n = 14) was infused intravenously. At 2 hours of reperfusion, regional cerebral blood flow using C-14-iodoantipyrine autoradiography, microregional arterial and venous (20-60 mm in diameter) O-2 saturation (SvO(2)) using cryomicrospectrophotometry, and the size of cortical infarction were determined. Results: Ischemia-reperfusion decreased microregional SvO(2) (52.9 +/- 3.7% vs. 61.1 +/- .6%, P < .005) with increased variation or heterogeneity (P < .0001) with similar regional cerebral blood flow and O-2 consumption. Dexmedetomidine during reperfusion decreased the heterogeneity of SvO(2) that was analyzed with an analysis of variance (P < .01) and reported as coefficient of variation (100 x standard deviation/Mean) (11.8 vs. 16.4). The number of veins with O-2 saturation less than 50% decreased with dexmedetomidine (13/80 vs. 27/81, P < .01). The percentage of cortical infarct in total cortex was smaller with dexmedetomidine (8.3 +/- 2.2% vs. 12.6 +/- 1.5%, P < .005). Conclusions: In the cerebral ischemic reperfused cortex, dexmedetomidine decreased the heterogeneity of SvO(2) and the number of small veins with low O-2 saturation suggesting improved microregional O-2 supply/consumption balance. The improvement was accompanied by the reduced size of cortical infarction.