Validation of Dexamethasone-Enhanced Continuous-Online Microdialysis for Monitoring Glucose for 10 Days after Brain Injury.

Validation of Dexamethasone-Enhanced Continuous-Online Microdialysis for Monitoring Glucose for 10 Days after Brain Injury.
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地塞米松增强连续在线微透析监测脑损伤后10天葡萄糖的验证。

DOI:
10.1021/acschemneuro.1c00231
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发表时间:
2021-10-06
影响因子:
5
通讯作者:
Michael, Adrian C.
Michael, Adrian C.
中科院分区:
医学3区
文献类型:
--
作者:
Gifford, Emily K.;Robbins, Elaine M.;Jaquins-Gerstl, Andrea;Rerick, Michael T.;Nwachuku, Enyinna L.;Weber, Stephen G.;Boutelle, Martyn G.;Okonkwo, David O.;Puccio, Ava M.;Michael, Adrian C.

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创伤性脑损伤(TBI)可引起一种病理生理状态,继发性损伤会加重这种状态。用颅内微透析监测脑代谢可以为减少颅脑损伤后的继发性损伤提供临床见解。最近对微透析的改进包括用于实时监测透析液样本流的连续工作的电化学生物传感器的实施,以及用于减轻组织对探针插入的反应的地塞米松反透析。地塞米松增强的持续在线微透析(地塞米松增强的COMD)记录了受控皮质撞击后大鼠血糖和患者脑外伤后血糖的长期下降。本研究采用反透析和荧光显微镜技术,探讨大鼠大脑皮质损伤后透析液葡萄糖下降的机制。这些发现证实了Dex增强的COMD在监测脑损伤后血糖方面的长期功能,证明了葡萄糖微透析与探针周围组织中的葡萄糖利用是偶联的,并验证了葡萄糖利用异常导致损伤后血糖下降的结论。
Traumatic brain injury (TBI) can induce a pathophysiologic state that is worsened by secondary injury. Monitoring brain metabolism with intracranial microdialysis can provide clinical insights to limit secondary injury in the days following TBI. Recent enhancements to microdialysis include the implementation of continuously-operating electrochemical biosensors for monitoring the dialysate sample stream in real time and dexamethasone retrodialysis to mitigate the tissue response to probe insertion. Dexamethasone-enhanced continuous-online microdialysis (Dex-enhanced coMD) records long-lasting declines of glucose after controlled cortical impact in rats and TBI in patients. The present study employs retrodialysis and fluorescence microscopy to investigate the mechanism responsible for the decline of dialysate glucose after injury of the rat cortex. The findings confirm the long-term functionality of Dex-enhanced coMD for monitoring brain glucose after injury, demonstrate that glucose microdialysis is coupled to glucose utilization in the tissues surrounding the probes, and validate the conclusion that aberrant glucose utilization drives the post-injury glucose decline.
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