Long-term hypothermia amplified neuroprotection by antagonizing intracranial pressure rebound after severe traumatic brain injury in rats.

IF 1.6 4区 医学 Q4 NEUROSCIENCES Neuroreport Pub Date : 2024-12-04 Epub Date: 2024-10-11 DOI:10.1097/WNR.0000000000002106
Xiaopeng Sun, Shugang Xu, Jingjing Wang, Xiaohong Li, Hongtao Sun, Wanyong Zhao
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Abstract

Long-term hypothermia has been reported to prevent intracranial pressure (ICP) rebound in clinical patients, but the duration for hypothermia and the corresponding ICP data are not available. This study investigated the optimal duration of long-term hypothermia in traumatic brain injury (TBI) rats, and observed the effect on ICP and neurological function. In this study, we established a rat severe TBI model with electronic Controlled Cortical Injury device, and implemented hypothermia (33 °C) for different durations. The motor function of the rats in each group was evaluated by beam walking test and inclined-grid climbing test, brain water content was calculated by the wet-dry weight method, Evan's blue staining was used to measure the blood-brain barrier (BBB) permeability, the change of hippocampal neurons was observed by Nissl staining, the expressions of BrdU, NeuN, and CD86 positive cells were detected by immunofluorescence staining, and the expressions of Bcl-2, Bax, iNOS, IL-10, and Arg-1 were detected by Western blot. We found that therapeutic hypothermia improved neurological recovery after TBI with declining ICP, reducing brain edema, decreasing BBB permeability, promoting neurogenesis, inhibiting apoptosis, and regulating inflammation. Moreover, 48 h hypothermia amplified the neuroprotective effect after injury on the basis of 4 or 24 h hypothermic treatment. Both 4 and 24 h hypothermia led to ICP rebound during or after rewarming, whereas 48 h hypothermia completely abolished ICP rebound. Our study suggests that long-term hypothermia amplifies neuroprotection after TBI by antagonizing ICP rebound.

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大鼠严重脑外伤后,长期低体温可通过拮抗颅内压反弹增强神经保护作用。
据报道,长期低体温可防止临床患者的颅内压(ICP)反弹,但低体温的持续时间和相应的ICP数据尚未获得。本研究探讨了创伤性脑损伤(TBI)大鼠长期低体温的最佳持续时间,并观察了其对 ICP 和神经功能的影响。在这项研究中,我们利用电子控制皮层损伤装置建立了大鼠严重创伤性脑损伤模型,并实施了不同持续时间的低体温(33 °C)。通过横梁行走试验和斜格爬行试验评估各组大鼠的运动功能,用干湿重量法计算脑含水量,用伊文氏蓝染色法测量血脑屏障(BBB)通透性、Nissl染色观察海马神经元的变化,免疫荧光染色检测BrdU、NeuN和CD86阳性细胞的表达,Western印迹检测Bcl-2、Bax、iNOS、IL-10和Arg-1的表达。我们发现,治疗性低温可改善创伤性脑损伤后的神经功能恢复,包括降低ICP、减轻脑水肿、降低BBB通透性、促进神经发生、抑制细胞凋亡和调节炎症。此外,48 小时低体温在 4 或 24 小时低体温治疗的基础上扩大了损伤后的神经保护作用。4 小时和 24 小时低体温都会导致复温时或复温后的 ICP 反弹,而 48 小时低体温则完全消除了 ICP 反弹。我们的研究表明,长期低体温可通过抑制ICP反弹来增强创伤性脑损伤后的神经保护作用。
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来源期刊
Neuroreport
Neuroreport 医学-神经科学
CiteScore
3.20
自引率
0.00%
发文量
150
审稿时长
1 months
期刊介绍: NeuroReport is a channel for rapid communication of new findings in neuroscience. It is a forum for the publication of short but complete reports of important studies that require very fast publication. Papers are accepted on the basis of the novelty of their finding, on their significance for neuroscience and on a clear need for rapid publication. Preliminary communications are not suitable for the Journal. Submitted articles undergo a preliminary review by the editor. Some articles may be returned to authors without further consideration. Those being considered for publication will undergo further assessment and peer-review by the editors and those invited to do so from a reviewer pool. The core interest of the Journal is on studies that cast light on how the brain (and the whole of the nervous system) works. We aim to give authors a decision on their submission within 2-5 weeks, and all accepted articles appear in the next issue to press.
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