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严重失血性休克患者的脑血流动力学变化与代谢改变。

Cerebral hemodynamic change and metabolic alteration in severe hemorrhagic shock.

机构信息

Britton Chance Center for Biomedical Photonics, Wuhan National Laboratory for Optoelectronics, Huazhong University of Science and Technology, Wuhan, 430074, P. R. China.

Key Laboratory of Biomedical Photonics of Ministry of Education, Department of Biomedical Engineering, Huazhong University of Science and Technology, Wuhan, 430074, P. R. China.

出版信息

Adv Exp Med Biol. 2014;812:217-223. doi: 10.1007/978-1-4939-0620-8_29.

Abstract

Understanding the biological mechanism and identifying biomarkers of hemorrhagic shock is important for diagnosis and treatment. We aim to use optical imaging to study how the cerebral blood circulation and metabolism change during the progression of severe hemorrhagic shock, especially the decompensatory stage. We used a multi-parameter (blood pressure (BP), cerebral blood flow (CBF), functional vascular density (FVD), blood oxygenation and mitochondrial NADH signal) cerebral cortex optical imaging system to observe brain hemodynamic change and metabolic alteration of rats in vivo for 4 h. Cerebral circulation and mitochondrial metabolism could be well preserved in the compensatory stage but impaired during the decompensatory stage. The changes of brain hemodynamics and metabolism may provide sensitive indicators for various shock stages including the transition from compensatory stage to decompensatory stage. Our novel imaging observations of hemodynamic and metabolic signals in vivo indicated that the rat brains under hemorrhagic shock suffered irreversible damage which could not be compensated by the autoregulation mechanism, probably due to injured mitochondria.

摘要

了解出血性休克的生物学机制和识别生物标志物对于诊断和治疗非常重要。我们旨在使用光学成像来研究严重出血性休克进展过程中(特别是失代偿期)大脑血液循环和代谢的变化。我们使用多参数(血压(BP)、脑血流量(CBF)、功能血管密度(FVD)、血氧和线粒体 NADH 信号)皮质脑光学成像系统观察了大鼠体内 4 小时的脑血流动力学变化和代谢改变。在代偿期,大脑循环和线粒体代谢可以得到很好的保存,但在失代偿期受到损害。脑血液动力学和代谢的变化可能为各种休克阶段提供敏感的指标,包括从代偿期到失代偿期的过渡。我们对活体血液动力学和代谢信号的新成像观察表明,出血性休克下的大鼠大脑受到不可逆转的损伤,可能由于受损的线粒体,自调节机制无法对此进行补偿。

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