Evolution of brain injury and neurological dysfunction after cardiac arrest in the rat - A multimodal and comprehensive model.

IF 4.9 2区医学 Q1 ENDOCRINOLOGY & METABOLISM Journal of Cerebral Blood Flow and Metabolism Pub Date : 2024-11-01 Epub Date: 2024-05-21 DOI:10.1177/0271678X241255599

Carlo Perego, Francesca Fumagalli, Francesca Motta, Marianna Cerrato, Edoardo Micotti, Davide Olivari, Daria De Giorgio, Giulia Merigo, Angelo Di Clemente, Alessandra Mandelli, Gianluigi Forloni, Luigi Cervo, Roberto Furlan, Roberto Latini, Robert W Neumar, Giuseppe Ristagno

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Abstract

Cardiac arrest (CA) is one of the leading causes of death worldwide. Due to hypoxic ischemic brain injury, CA survivors may experience variable degrees of neurological dysfunction. This study, for the first time, describes the progression of CA-induced neuropathology in the rat. CA rats displayed neurological and exploratory deficits. Brain MRI revealed cortical and striatal edema at 3 days (d), white matter (WM) damage in corpus callosum (CC), external capsule (EC), internal capsule (IC) at d7 and d14. At d3 a brain edema significantly correlated with neurological score. Parallel neuropathological studies showed neurodegeneration, reduced neuronal density in CA1 and hilus of hippocampus at d7 and d14, with cells dying at d3 in hilus. Microgliosis increased in cortex (Cx), caudate putamen (Cpu), CA1, CC, and EC up to d14. Astrogliosis increased earlier (d3 to d7) in Cx, Cpu, CC and EC compared to CA1 (d7 to d14). Plasma levels of neurofilament light (NfL) increased at d3 and remained elevated up to d14. NfL levels at d7 correlated with WM damage. The study shows the consequences up to 14d after CA in rats, introducing clinically relevant parameters such as advanced neuroimaging and blood biomarker useful to test therapeutic interventions in this model.

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大鼠心脏骤停后脑损伤和神经功能障碍的演变--一个多模式综合模型。

心脏骤停（CA）是导致全球死亡的主要原因之一。由于缺氧缺血性脑损伤，心脏骤停幸存者可能会出现不同程度的神经功能障碍。本研究首次描述了 CA 引起的大鼠神经病理学进展。CA 大鼠表现出神经和探索功能障碍。脑磁共振成像显示，大鼠3天（d）时皮质和纹状体水肿，7天（d7）和14天（d14）时胼胝体（CC）、外囊（EC）和内囊（IC）的白质（WM）受损。d3 脑水肿与神经系统评分明显相关。同时进行的神经病理学研究显示，d7和d14时，神经变性、海马CA1和后部神经元密度降低，d3时后部细胞死亡。皮质（Cx）、尾状核丘脑（Cpu）、CA1、CC和EC的小胶质细胞增多，直至d14。Cx、Cpu、CC和EC的星形胶质细胞增多（d3至d7）早于CA1（d7至d14）。血浆中的神经丝光（NfL）水平在d3时升高，并在d14时保持升高。d7 的 NfL 水平与 WM 损伤相关。该研究显示了大鼠CA发生后14天内的后果，引入了临床相关参数，如先进的神经影像学和血液生物标记物，有助于在该模型中测试治疗干预措施。

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来源期刊

Journal of Cerebral Blood Flow and Metabolism 医学-内分泌学与代谢

CiteScore

12.00

自引率

4.80%

发文量

300

审稿时长

3 months

期刊介绍： JCBFM is the official journal of the International Society for Cerebral Blood Flow & Metabolism, which is committed to publishing high quality, independently peer-reviewed research and review material. JCBFM stands at the interface between basic and clinical neurovascular research, and features timely and relevant research highlighting experimental, theoretical, and clinical aspects of brain circulation, metabolism and imaging. The journal is relevant to any physician or scientist with an interest in brain function, cerebrovascular disease, cerebral vascular regulation and brain metabolism, including neurologists, neurochemists, physiologists, pharmacologists, anesthesiologists, neuroradiologists, neurosurgeons, neuropathologists and neuroscientists.