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二氧化碳在大鼠急性脑卒中半暗带中的作用

The Role of Carbon Dioxide in the Rat Acute Stroke Penumbra.

作者信息

Yeo Leonard L, Arnberg Fabian, Chireh Arvin, Sharma Vijay, Tan Benjamin, Gontu Vamsi, Little Philip, Holmin Staffan

机构信息

Departments of Neuroradiology, Karolinska University Hospital, Stockholm, Sweden.

Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.

出版信息

Front Digit Health. 2022 Feb 4;3:824334. doi: 10.3389/fdgth.2021.824334. eCollection 2021.

Abstract

PURPOSE

The vasodilatory response to inhaled CO occurs in the acute stroke ischemic penumbra and may be a potential therapeutic modality.

METHODS

Twenty-two Sprague-Dawley rats were subjected to 90-min occlusion of the M2 segment of the middle cerebral artery (M2CAO) by endovascular technique. The animals were administered different C02 concentrations and scanned serially with 9.4 T MRI. Infarct tissue was determined by diffusion-weighted imaging (DWI) and hypoperfused tissue was determined by arterial spin labeling (PWI).

RESULTS

4 animals were administered room air (RA)+ 6% CO (group 1), 6 animals RA+12% CO (Group 2) and 4 animals only RA (group 3). In the rats with CO administered (groups 1 and 2), the DWI lesion to cerebral hypoperfusion volume ratio (SD) at pre-CO administration, was 0.145(0.168), which increased to 0.708(0.731) during CO administration and reduced to 0.533(0.527) post-CO administration. In 9 of 10 rats the hypoperfused volume decreased when CO was administered. When CO was stopped the hypoperfused volume became larger again. Administration of RA+12% CO (Group 2) decreased the volume of CBF hypoperfusion significantly compared to the control group (95%CI: 0.084 ± 0.0213, = 0.004).

CONCLUSION

Inhaled CO appears to reduce the size of the hypoperfused tissue volume during acute stroke and may be a potential modality for treatment of acute ischemic stroke. These findings will nonetheless need to be validated in a larger cohort in other centers.

摘要

目的

吸入一氧化碳(CO)后的血管舒张反应发生在急性脑卒中缺血半暗带,可能是一种潜在的治疗方式。

方法

采用血管内技术对22只Sprague-Dawley大鼠大脑中动脉M2段进行90分钟闭塞(M2CAO)。给动物吸入不同浓度的CO2,并采用9.4T磁共振成像(MRI)进行连续扫描。通过扩散加权成像(DWI)确定梗死组织,通过动脉自旋标记(PWI)确定灌注不足组织。

结果

4只动物吸入室内空气(RA)+6%CO(第1组),6只动物吸入RA+12%CO(第2组),4只动物仅吸入RA(第3组)。在吸入CO的大鼠(第1组和第2组)中,吸入CO前DWI病变与脑灌注不足体积比(SD)为0.145(0.168),吸入CO期间增加至0.708(0.731),吸入CO后降至0.533(0.527)。10只大鼠中有9只在吸入CO时灌注不足体积减小。当停止吸入CO时,灌注不足体积再次增大。与对照组相比,吸入RA+12%CO(第2组)显著降低了脑血流量灌注不足的体积(95%CI:0.084±0.0213,P=0.004)。

结论

吸入CO似乎可减小急性脑卒中期间灌注不足组织体积的大小,可能是治疗急性缺血性脑卒中的一种潜在方式。然而,这些发现仍需在其他中心的更大队列中进行验证。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea52/8854855/ea1b8dacbb62/fdgth-03-824334-g0001.jpg

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