Wang Shaoxun, Roman Richard J, Fan Fan
Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, MS 39216, USA.
J Neurobiol Physiol. 2020;2(1):15-18. doi: 10.46439/neurobiology.2.008.
Individuals with spinal cord injury (SCI) have a significantly increased risk for cognitive impairment that is associated with cerebrovascular remodeling and endothelial dysfunction. The sub-acute stage following high thoracic SCI is characterized by increased fibrosis and stiffness of cerebral arteries. However, a more prolonged duration after SCI exacerbates cerebrovascular injury by damaging endothelium. Endothelial dysfunction is associated with reduced expression of transient receptor potential cation channel 4 that mediates the production of nitric oxide and epoxyeicosatrienoic acids following shear stress and the response to carbachol and other endothelium-dependent vasodilators. Reduced expression of CD31 in cerebral arteries also suggests the loss of endothelial cell integrity following chronic SCI. Repetitively transient hypertension and intermittent hypotension contribute to cerebrovascular endothelial dysfunction in the animals with a sub-acute stage of high thoracic SCI. The increase in vascular remodeling and endothelial dysfunction ultimately reduce cerebral blood flow, which promotes cerebral hypoperfusion and cognitive dysfunction in the chronic phase of SCI. In conclusion, the duration and magnitude of fluctuations in blood pressure after SCI play a vital role in the onset and progress of cerebrovascular dysfunction, which promotes the development of cognitive impairment.
脊髓损伤（SCI）患者出现认知障碍的风险显著增加，这与脑血管重塑和内皮功能障碍有关。高胸段脊髓损伤后的亚急性期，其特征是脑动脉纤维化和僵硬程度增加。然而，脊髓损伤后更长的时间会通过损伤内皮加剧脑血管损伤。内皮功能障碍与瞬时受体电位阳离子通道4表达减少有关，该通道介导剪切应力后一氧化氮和环氧二十碳三烯酸的产生以及对卡巴胆碱和其他内皮依赖性血管舒张剂的反应。脑动脉中CD31表达减少也表明慢性脊髓损伤后内皮细胞完整性丧失。反复短暂高血压和间歇性低血压会导致高胸段脊髓损伤亚急性期动物出现脑血管内皮功能障碍。血管重塑和内皮功能障碍的增加最终会减少脑血流量，从而在脊髓损伤的慢性期促进脑灌注不足和认知功能障碍。总之，脊髓损伤后血压波动的持续时间和幅度在脑血管功能障碍的发生和发展中起着至关重要的作用，进而促进认知障碍的发展。
