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水中毒诱发的细胞毒性脑水肿以及渗透性血脑屏障破坏诱发的血管源性脑水肿,在对自由活动大鼠进行遥测监测期间会导致不同的颅内压升高模式。

Cytotoxic brain edema induced by water intoxication and vasogenic brain edema induced by osmotic BBB disruption lead to distinct pattern of ICP elevation during telemetric monitoring in freely moving rats.

作者信息

Kozler Petr, Maresova Dana, Pokorny Jaroslav

机构信息

Institute of Physiology, First Faculty of Medicine, Charles University in Prague, Prague, Czech Republic.

出版信息

Neuro Endocrinol Lett. 2019 Dec;40(6):249-256.

Abstract

OBJECTIVES

A novel method of long-term telemetric monitoring of mean arterial pressure (MAP) and intracranial pressure (ICP) for the determination of current cerebral perfusion pressure (CPP) and the time course of ICP in freely moving rats under physiological conditions and with increased ICP due to the induced cerebral edema were studied.

METHODS

The brain edema, that caused volume enlargement and ICP elevation was achieved in entirely experimental conditions without any parallel pathological process. Vasogenic/extracellular edema was induced by osmotic blood-brain barrier disruption (BBBd) and for induction of cytotoxic/intracellular edema the water intoxication model (WI) was used.

RESULTS

The results showed significantly elevated values of ICP both in conditions of osmotic blood-brain barrier disruption (BBBd model) and cytotoxic/intracellular edema (WI model) compared to intact rats. The average values of ICP were significantly higher in WI model compared to osmotic BBBd model. Distinct pattern of elevated ICP, related to the selected way of experimental brain edema induction, was found. In the experimental model of osmotic BBB disruption, the elevation of ICP started earlier but was of very short duration. In WI model the elevation of ICP was present during the whole period of monitoring.

CONCLUSION

Our results indicate that purely experimental models of brain edema (WI, BBBd) without any parallel pathological process can compromise the basic brain homeostatic activity.

摘要

目的

研究一种用于长期遥测平均动脉压(MAP)和颅内压(ICP)的新方法,以测定在生理条件下以及因诱导性脑水肿导致颅内压升高时自由活动大鼠的当前脑灌注压(CPP)和颅内压随时间的变化过程。

方法

在完全实验条件下实现导致体积增大和颅内压升高的脑水肿,且无任何并发的病理过程。通过渗透性血脑屏障破坏(BBBd)诱导血管源性/细胞外水肿,使用水中毒模型(WI)诱导细胞毒性/细胞内水肿。

结果

结果显示,与完整大鼠相比,在渗透性血脑屏障破坏(BBBd模型)和细胞毒性/细胞内水肿(WI模型)情况下,颅内压值均显著升高。WI模型中的颅内压平均值显著高于渗透性BBBd模型。发现了与所选实验性脑水肿诱导方式相关的不同颅内压升高模式。在渗透性血脑屏障破坏的实验模型中,颅内压升高开始得较早,但持续时间很短。在WI模型中,颅内压在整个监测期间都存在升高。

结论

我们的结果表明,没有任何并发病理过程的纯实验性脑水肿模型(WI,BBBd)可能会损害大脑的基本稳态活动。

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