Stroke:优降糖预防恶性水肿的机制

2020-02-27 杨中华 脑血管病及重症文献导读

最近发现在动物实验和人类中平扫 CT 定量放射强度(radiodensity)可以作为缺血性卒中病灶内水摄取的评价工具。最近几项研究显示定量放射强度测量法是一种与缺血性卒中病灶、心脏骤停后和儿科创伤性脑损伤有关的标志物。

大面积半球梗死(large hemispheric infarction,LHI)后脑水肿是缺血性卒中的严重并发症,会引起神经功能恶化。恶性脑水肿通常出现在卒中后2-4天,与临床状态加重有关,比如意识水平下降。尽管它仅占卒中患者的2-8%,但是在 LHI 患者中恶性水肿的发生率高达32%-50%。离子通道功能障碍和血脑屏障破坏引起离子梯度变化,这样会引起过多的水分聚集,这是恶性水肿的可能发病机制。换句话说,过量的水分会引起病灶水肿和占位效应,这也会对临近正常脑组织造成破坏。

几种方法能够测量占位效应,最常用的方法为中线移位(midline shift,MLS),很少有研究采用影像学技术直接测量水含量。相较而言,最近发现在动物实验和人类中平扫 CT 定量放射强度(radiodensity)可以作为缺血性卒中病灶内水摄取的评价工具。最近几项研究显示定量放射强度测量法是一种与缺血性卒中病灶、心脏骤停后和儿科创伤性脑损伤有关的标志物。

临床前的研究显示 SRU1(磺脲类受体1)-调节离子通道参与了卒中后离子型和血管源性水肿的形成过程。静脉内输注优降糖通过抑制 SUR1能够防止卒中动物模型的脑内水蓄积,减轻占位效应。

在本研究中,我们探讨了一些治疗措施是否能够改变患者的水摄取,是否可以把水摄取作为脑水肿研究的潜在中间终点。我们对 GAMES-RP 试验中的患者做了研究,利用系列 CT 扫描比较安慰剂治疗组和静脉输注优降糖治疗组的水净摄取(net water uptake,NWU)。

该研究的目的在于通过脑水肿的影像学标志物探讨静脉输注优降糖的机制。我们首次探讨并定义了水摄取、占位效应的时间过程和动力学,确定初始的水摄取值是否能够预测随后的恶性水肿。最后,我们探讨了静脉输注优降糖是否能够随着时间改变脑水肿形成的轨迹。我们试验假设脑水肿的形成会开始聚集,并进入平台期,SUR1抑制将能够减轻水肿的形成。

这是 GAMRES-RP 试验的事后探索性分析。对GAMES-RP 试验改良 ITT 样本给药当天和第7天(n = 264)的平扫 CT进行分析。测量CT 的放射强度(即,NWU)和中线移位(MLS)的定量变化。灰白质的 NWU 也分别被验讫。重复-测量混合-效应模型(Repeated-measures mixed-effects models)被用于评价静脉输注优降糖对 MLS 和 NWU 的作用。

卒中后前7天内平均进行了3次 CT 扫描。在重复-测量回归模型中,更加明显的 NWU 与 增加的MLS 有关(β=0.23; 95% CI, 0.20–0.26; P<0.001)。静脉输注优降糖与 NWU 降低(β=?2.80; 95% CI, ?5.07 to ?0.53; P=0.016)以及 MLS 减轻(β=?1.50; 95% CI, ?2.71 to ?0.28; P=0.016)有关。静脉输注优降糖能够降低灰白质水的摄取。在中间分析中(In mediation analysis),灰质 NWU(β=0.15; 95% CI, 0.11–0.20; P<0.001)对 MLS 占位效应的影响高于白质 NWU。

在这项2期事后分析中,静脉输注优降糖能够降低大面积半球梗死后的水蓄积和占位效应。该研究显示 NWU 是一种量化和可变的缺血性脑水肿蓄积的标志物。

原始出处:Pongpat Vorasayan, Matthew B. Bevers, Lauren A. Beslow, et al. Intravenous Glibenclamide Reduces Lesional Water Uptake in Large Hemispheric Infarction. Stroke. 20 Sep 2019

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    2020-09-08 whmdzju
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    2020-02-29 jin321

    这也可以?

    0

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    2020-02-28 小华子
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    2020-02-28 thm112988

    0

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    2020-02-27 njwbhuang

    学习了好的知识,感谢!

    0

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    2020-02-27 肿肿

    机制研究离临床仍然有距离,不过与临床结合思考,仍然有帮助的,不能仅仅是纯临床思维,转化思维同样重要

    0

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