Exercise-induced oxidative-nitrosative stress is associated with impaired dynamic cerebral autoregulation and blood-brain barrier leakage

Exercise-induced oxidative-nitrosative stress is associated with impaired dynamic cerebral autoregulation and blood-brain barrier leakage
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DOI:
10.1113/expphysiol.2011.060178
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发表时间:
2011-11-01
影响因子:
2.7
通讯作者:
Pietri, Sylvia
Pietri, Sylvia
中科院分区:
医学4区
文献类型:
--
作者:
Bailey, Damian M.;Evans, Kevin A.;Pietri, Sylvia

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本研究考察了动态脑自动调节和血脑屏障功能是否会因运动引起的氧化应激而受到损害。研究人员对8名健康男性进行了检查,他们分别在休息状态和半平躺式自行车运动后进行了检查,直到精疲力竭。通过连续记录大脑中动脉血流速度(MCAv)和短暂性低血压期间的平均动脉压,确定恢复过程中动态大脑自动调节指数的变化。采用电子顺磁共振波谱法和臭氧化学发光法直接检测静脉血中自旋俘获自由基和一氧化氮代谢物。ELISA法检测神经元特异性烯醇化酶、S100 β和3-硝基酪氨酸。虽然运动没有改变MCAv,但它引起了自调节指数的轻度降低(从6.9 +/- 0.6降至5.5 +/- 0.9 a.u, P < 0.05),这与运动引起的抗坏血酸自由基、5-(二氧基磷酰)-5-甲基-1-吡啶n -氧化物和n -叔丁基-a-苯基硝基酮加合物、3-硝基酪氨酸和S100 β的增加直接相关(r=0.66至0.76,P < 0.05)。相反,未观察到神经元特异性烯醇化酶的变化。总之,我们的研究结果表明,剧烈运动有可能增加血脑屏障的通透性,而不会导致自由基介导的动态大脑自动调节损伤后的结构性脑损伤。
The present study examined whether dynamic cerebral autoregulation and bloodbrain barrier function would become compromised as a result of exercise-induced oxidativenitrosative stress. Eight healthy men were examined at rest and after an incremental bout of semi-recumbent cycling exercise to exhaustion. Changes in a dynamic cerebral autoregulation index were determined during recovery from continuous recordings of blood flow velocity in the middle cerebral artery (MCAv) and mean arterial pressure during transiently induced hypotension. Electron paramagnetic resonance spectroscopy and ozone-based chemiluminescence were employed for direct detection of spin-trapped free radicals and nitric oxide metabolites in venous blood. Neuron-specific enolase, S100 beta and 3-nitrotyrosine were determined by ELISA. While exercise did not alter MCAv, it caused a mild reduction in the autoregulation index (from 6.9 +/- 0.6 to 5.5 +/- 0.9 a.u., P < 0.05) that correlated directly against the exercise-induced increase in the ascorbate radical, 5-(diethoxyphosphoryl)-5-methyl-1-pyrroline N-oxide and N-tert-butyl-a-phenylnitrone adducts, 3-nitrotyrosine and S100 beta (r=0.66 to 0.76, P < 0.05). In contrast, no changes in neuron-specific enolase were observed. In conclusion, our findings suggest that intense exercise has the potential to increase bloodbrain barrier permeability without causing structural brain damage subsequent to a free radical-mediated impairment in dynamic cerebral autoregulation.