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- Tao Yang, Ziwen Lu, Lei Wang, Yizhou Zhao, Binbin Nie, Qing Xu, Xiaowan Han, Tong Li, Jiuli Zhao, Wenkun Cheng, Baofu Wang, Aiming Wu, Haiyan Zhu, Wei Meng, Hongcai Shang, and Mingjing Zhao.
- Key Laboratory of Chinese Internal Medicine of Ministry of Education and Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, China.
- Neuroscience. 2020 Jan 1; 424: 34-44.
AbstractPatients with heart failure (HF) are more susceptible to cognitive impairment, but the mechanism is still unclear. This study aimed to observe the dynamic changes in brain glucose metabolism and neuronal structure in different stages of HF. An HF rat model was established by ligating the anterior descending branch of the left coronary artery. To simulate acute heart failure (AHF) and chronic heart failure (CHF) in the clinic, relevant laboratory indexes were detected 10 and 60 days after ligation. The results showed that the model rats had systolic HF. Cognitive function was not obviously impaired in 10-day rats with HF, while the memory and learning functions were significantly impaired in 60-day rats with HF. The brain glucose metabolism in 10-day rats compensatorily increased in the prefrontal cortex (PFC), medial PFC (mPFC), cingulate gyrus, and basal ganglia (BG). In contrast, the metabolism of 60-day rats reduced in the PFC and BG. Meanwhile, the neuronal structure slightly changed in 10-day rats with HF, but neuronal karyopyknosis, reduced Nissl bodies, and swollen organelles were found in 60-day rats with HF. In conclusion, brain glucose metabolism and neuronal structure showed a dynamic evolution. Rats with AHF were in a compensatory state for increased glucose metabolism and slight neuronal damage. As a result, no significant cognitive impairment was observed. However, rats with CHF had significantly decreased cerebral glucose metabolism and neuronal degeneration, contributing to the cognitive function after HF.Copyright © 2019 The Author(s). Published by Elsevier Ltd.. All rights reserved.
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