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颅脑创伤后的脑代谢紊乱。

Cerebral metabolic derangements following traumatic brain injury.

机构信息

Division of Anaesthesia, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK.

Department of Anesthesiology and Critical Care, CHU de Québec-Université Laval, Quebec City, Quebec, Canada.

出版信息

Curr Opin Anaesthesiol. 2022 Oct 1;35(5):562-569. doi: 10.1097/ACO.0000000000001183. Epub 2022 Aug 18.

DOI:10.1097/ACO.0000000000001183
PMID:35943124
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9594147/
Abstract

PURPOSE OF REVIEW

Outcome following traumatic brain injury (TBI) remains variable, and derangements in cerebral metabolism are a common finding in patients with poor outcome. This review compares our understanding of cerebral metabolism in health with derangements seen following TBI.

RECENT FINDINGS

Ischemia is common within the first 24 h of injury and inconsistently detected by bedside monitoring. Metabolic derangements can also result from tissue hypoxia in the absence of ischemic reductions in blood flow due to microvascular ischemia and mitochondrial dysfunction. Glucose delivery across the injured brain is dependent on blood glucose and regional cerebral blood flow, and is an important contributor to derangements in glucose metabolism. Alternative energy substrates such as lactate, ketone bodies and succinate that may support mitochondrial function, and can be utilized when glucose availability is low, have been studied following TBI but require further investigation.

SUMMARY

Mitochondrial dysfunction and the use of alternative energy substrates are potential therapeutic targets, but improved understanding of the causes, impact and significance of metabolic derangements in clinical TBI are needed. Maintaining adequate oxygen and glucose delivery across the injured brain may accelerate the recovery of mitochondrial function and cerebral energy metabolism and remain important management targets.

摘要

目的综述

创伤性脑损伤(TBI)后的结果仍然存在差异,并且脑代谢紊乱是预后不良患者的常见发现。本综述比较了我们对健康状态下大脑代谢的理解与 TBI 后观察到的代谢紊乱。

最近的发现

伤后 24 小时内缺血很常见,但通过床边监测不能一致地检测到。代谢紊乱也可能由于微血管缺血和线粒体功能障碍导致血流无缺血性减少而导致组织缺氧。损伤大脑的葡萄糖输送依赖于血糖和局部脑血流量,并且是葡萄糖代谢紊乱的重要贡献者。在 TBI 后已经研究了乳酸、酮体和琥珀酸等替代能量底物,这些底物可以支持线粒体功能,并且在葡萄糖供应不足时可以利用,但是需要进一步研究。

总结

线粒体功能障碍和替代能量底物的使用是潜在的治疗靶点,但是需要更好地了解代谢紊乱在临床 TBI 中的原因、影响和意义。保持损伤大脑的足够氧和葡萄糖输送可能会加速线粒体功能和脑能量代谢的恢复,仍然是重要的管理目标。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12d/9594147/e9dc0882e924/coana-35-562-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12d/9594147/7b44bc632e34/coana-35-562-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12d/9594147/35dcbbeefea7/coana-35-562-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12d/9594147/c6984411805f/coana-35-562-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12d/9594147/73edc8f9c443/coana-35-562-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12d/9594147/e9dc0882e924/coana-35-562-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12d/9594147/7b44bc632e34/coana-35-562-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12d/9594147/35dcbbeefea7/coana-35-562-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12d/9594147/c6984411805f/coana-35-562-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12d/9594147/73edc8f9c443/coana-35-562-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12d/9594147/e9dc0882e924/coana-35-562-g005.jpg

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