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脑血流和组织代谢物的时程变化表明,在大鼠实验性蛛网膜下腔出血后存在持续的代谢抑制。

The temporal profile of cerebral blood flow and tissue metabolites indicates sustained metabolic depression after experimental subarachnoid hemorrhage in rats.

机构信息

Department of Neurosurgery, University of Würzburg, Würzburg, Germany.

出版信息

Neurosurgery. 2011 Jan;68(1):223-9; discussion 229-30. doi: 10.1227/NEU.0b013e3181fe23c1.

DOI:10.1227/NEU.0b013e3181fe23c1
PMID:21099709
Abstract

BACKGROUND

Derangement of cerebral metabolism occurs after various insults such as ischemia, traumatic brain injury, and subarachnoid hemorrhage (SAH).

OBJECTIVE

To investigate the course of cerebral blood flow and metabolic parameters in the first hours after experimental SAH.

METHODS

Sixteen Sprague-Dawley rats were subjected to SAH using the endovascular filament model or served as controls (8 rats in each group). Local cerebral blood flow and intracranial pressure were measured continuously. Microdialysis samples were acquired in 30-minute intervals for 6 hours after SAH. Concentrations of glucose, lactate, pyruvate, and glutamate were determined.

RESULTS

After induction of SAH, cerebral perfusion pressure and local cerebral blood flow sharply decreased. The decrease in local cerebral blood flow exceeded the decrease in cerebral perfusion pressure throughout the observation period. Glutamate concentrations in microdialysis samples increased sixfold and recovered to baseline levels. Lactate concentrations immediately increased after SAH, recovered incompletely, and remained above the levels of control animals until the end of the sampling period. Pyruvate concentrations showed a delayed increase starting 2 hours after SAH.

CONCLUSION

The course of cerebral blood flow after SAH resembles global ischemia followed by a continuous low-flow state caused by a sudden decrease in cerebral perfusion pressure and acute vasoconstriction. The courses of lactate and pyruvate concentrations indicate a persistently deranged aerobic metabolism.

摘要

背景

在各种损伤后,如缺血、脑外伤和蛛网膜下腔出血(SAH),会发生脑代谢紊乱。

目的

研究实验性 SAH 后最初数小时内脑血流和代谢参数的变化过程。

方法

16 只 Sprague-Dawley 大鼠采用血管内纤维蛋白模型制作 SAH 模型,或作为对照组(每组 8 只)。连续测量局部脑血流和颅内压。SAH 后以 30 分钟为间隔采集微透析样本,持续 6 小时。测定葡萄糖、乳酸、丙酮酸和谷氨酸浓度。

结果

在 SAH 诱导后,脑灌注压和局部脑血流量急剧下降。在整个观察期间,局部脑血流量的下降超过脑灌注压的下降。微透析样本中谷氨酸浓度增加了 6 倍,并恢复到基线水平。SAH 后乳酸浓度立即升高,不完全恢复,直至采样结束时仍高于对照组动物的水平。丙酮酸浓度在 SAH 后 2 小时开始延迟增加。

结论

SAH 后脑血流的变化过程类似于全脑缺血,随后由于脑灌注压突然下降和急性血管收缩,导致持续的低血流状态。乳酸和丙酮酸浓度的变化过程表明有氧代谢持续紊乱。

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