目的观察基于相位对比(PC)MRI颅内血流动力学参数预测急性高原反应(AMS)的价值。方法前瞻性招募72名健康青年志愿者,于平原地区采集平静呼吸及轻、中及重度瓦尔萨尔瓦动作(VM)下的颈内动脉(ICA)及颈内静脉(IJV)PC MRI并记录ICA及IJV血...目的观察基于相位对比(PC)MRI颅内血流动力学参数预测急性高原反应(AMS)的价值。方法前瞻性招募72名健康青年志愿者,于平原地区采集平静呼吸及轻、中及重度瓦尔萨尔瓦动作(VM)下的颈内动脉(ICA)及颈内静脉(IJV)PC MRI并记录ICA及IJV血流动力学参数;根据急进海拔4411 m的高原地区10 h后路易斯湖评分(LLS)结果划分AMS组(n=9)与无AMS组(n=63);采用单因素及多因素logistic回归分析筛选各状态下AMS的独立预测因素,构建单一及联合VM状态预测模型;绘制受试者工作特征曲线,计算曲线下面积(AUC),评估各模型预测效能。结果轻度VM下ICA搏动指数(PI ICA)、中度VM下IJV面积(S IJV)及重度VM下IJV阻力指数(RI IJV)均为AMS独立预测因素(P均<0.05)。联合VM状态模型(AUC=0.869)预测AMS的效能高于单一VM状态模型(AUC=0.698~0.738)。结论基于轻度VM PI ICA、中度VM S IJV及重度VM RI IJV构建的模型可有效预测AMS。展开更多
Objective High-altitude hypoxia exposure often damages hippocampus-dependent learning and memory.Nogo-A is an important axonal growth inhibitory factor.However,its function in high-altitude hypoxia and its mechanism o...Objective High-altitude hypoxia exposure often damages hippocampus-dependent learning and memory.Nogo-A is an important axonal growth inhibitory factor.However,its function in high-altitude hypoxia and its mechanism of action remain unclear.Methods In an in vivo study,a low-pressure oxygen chamber was used to simulate high-altitude hypoxia,and genetic or pharmacological intervention was used to block the Nogo-A/NgR1 signaling pathway.Contextual fear conditioning and Morris water maze behavioral tests were used to assess learning and memory in rats,and synaptic damage in the hippocampus and changes in oxidative stress levels were observed.In vitro,SH-SY5Y cells were used to assess oxidative stress and mitochondrial function with or without Nogo-A knockdown in Oxygen Glucose-Deprivation/Reperfusion(OGD/R)models.Results Exposure to acute high-altitude hypoxia for 3 or 7 days impaired learning and memory in rats,triggered oxidative stress in the hippocampal tissue,and reduced the dendritic spine density of hippocampal neurons.Blocking the Nogo-A/NgR1 pathway ameliorated oxidative stress,synaptic damage,and the learning and memory impairment induced by high-altitude exposure.Conclusion Our results demonstrate the detrimental role of Nogo-A protein in mediating learning and memory impairment under high-altitude hypoxia and suggest the potential of the Nogo-A/NgR1 signaling pathway as a crucial therapeutic target for alleviating learning and memory dysfunction induced by high-altitude exposure.展开更多
文摘目的观察基于相位对比(PC)MRI颅内血流动力学参数预测急性高原反应(AMS)的价值。方法前瞻性招募72名健康青年志愿者,于平原地区采集平静呼吸及轻、中及重度瓦尔萨尔瓦动作(VM)下的颈内动脉(ICA)及颈内静脉(IJV)PC MRI并记录ICA及IJV血流动力学参数;根据急进海拔4411 m的高原地区10 h后路易斯湖评分(LLS)结果划分AMS组(n=9)与无AMS组(n=63);采用单因素及多因素logistic回归分析筛选各状态下AMS的独立预测因素,构建单一及联合VM状态预测模型;绘制受试者工作特征曲线,计算曲线下面积(AUC),评估各模型预测效能。结果轻度VM下ICA搏动指数(PI ICA)、中度VM下IJV面积(S IJV)及重度VM下IJV阻力指数(RI IJV)均为AMS独立预测因素(P均<0.05)。联合VM状态模型(AUC=0.869)预测AMS的效能高于单一VM状态模型(AUC=0.698~0.738)。结论基于轻度VM PI ICA、中度VM S IJV及重度VM RI IJV构建的模型可有效预测AMS。
基金supported by Beijing Natural Science Foundation(No.7232090)the National Natural Science Foundation of China(82101306)the Scientific and Technological Innovation 2030(2021ZD0201100).
文摘Objective High-altitude hypoxia exposure often damages hippocampus-dependent learning and memory.Nogo-A is an important axonal growth inhibitory factor.However,its function in high-altitude hypoxia and its mechanism of action remain unclear.Methods In an in vivo study,a low-pressure oxygen chamber was used to simulate high-altitude hypoxia,and genetic or pharmacological intervention was used to block the Nogo-A/NgR1 signaling pathway.Contextual fear conditioning and Morris water maze behavioral tests were used to assess learning and memory in rats,and synaptic damage in the hippocampus and changes in oxidative stress levels were observed.In vitro,SH-SY5Y cells were used to assess oxidative stress and mitochondrial function with or without Nogo-A knockdown in Oxygen Glucose-Deprivation/Reperfusion(OGD/R)models.Results Exposure to acute high-altitude hypoxia for 3 or 7 days impaired learning and memory in rats,triggered oxidative stress in the hippocampal tissue,and reduced the dendritic spine density of hippocampal neurons.Blocking the Nogo-A/NgR1 pathway ameliorated oxidative stress,synaptic damage,and the learning and memory impairment induced by high-altitude exposure.Conclusion Our results demonstrate the detrimental role of Nogo-A protein in mediating learning and memory impairment under high-altitude hypoxia and suggest the potential of the Nogo-A/NgR1 signaling pathway as a crucial therapeutic target for alleviating learning and memory dysfunction induced by high-altitude exposure.
