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大鼠脑缺血后积水与缺血后延迟性低灌注有关吗?

Is postischaemic water accumulation related to delayed postischaemic hypoperfusion in rat brain?

作者信息

Schürer L, Grögaard B, Arfors K E, Gerdin B

机构信息

Institute for Surgical Research, Ludwig-Maximilians-University of Munich, Klinikum Grosshadern, Federal Republic of Germany.

出版信息

Acta Neurochir (Wien). 1988;94(3-4):150-4. doi: 10.1007/BF01435869.

Abstract

The effect of reversible cerebral ischaemia on brain oedema development was studied with a gravimetric method. Cerebral blood flow changes after ischaemia were correlated with alterations in brain specific gravity. Forebrain ischaemia (15 min) was induced in rats by reversible bilateral ligation of both carotid arteries plus induction of controlled hypotension to 50 mm Hg. The specific gravity of different brain structures was determined in a Percoll column up to 24 h after ischaemia. In addition, regional cerebral blood flow was measured by 14C-iodoantipyrine autoradiography. Cerebral ischaemia resulted in reduction of cerebral blood flow to less than 1% of normal in cortical structures and the caudatoputamen. One hour after the end of ischaemia blood flows were still reduced to 30-50% of the control level indicative of delayed postischaemic hypoperfusion. Specific gravity in cortex and hypothalamus reached a maximal decrease 10 min after the end of the ischaemia, and was still significantly reduced at 1 h, while it was normal again 6 hrs later. Regression analysis between regional cerebral blood flows and the corresponding specific gravities were made at various time points, but no significant correlations could be established. Other mechanisms, like vasoconstriction, rheologic or metabolic factors may be causative for the delayed postischaemic hypoperfusion.

摘要

采用重量法研究了可逆性脑缺血对脑水肿发展的影响。缺血后脑血流量的变化与脑比重的改变相关。通过双侧颈动脉可逆性结扎并将控制性低血压诱导至50 mmHg,在大鼠中诱导前脑缺血(15分钟)。在缺血后长达24小时内,在Percoll柱中测定不同脑结构的比重。此外,通过14C-碘安替比林放射自显影术测量局部脑血流量。脑缺血导致皮质结构和尾状核壳核的脑血流量减少至正常的1%以下。缺血结束1小时后,血流量仍降至对照水平的30-50%,表明存在缺血后延迟性低灌注。皮质和下丘脑的比重在缺血结束后10分钟达到最大降低,1小时时仍显著降低,而6小时后恢复正常。在不同时间点对局部脑血流量和相应比重进行回归分析,但未建立显著相关性。其他机制,如血管收缩、流变学或代谢因素,可能是缺血后延迟性低灌注的原因。

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