Psychological stress-induced cerebrovascular dysfunction: the role of metabolic syndrome and exercise.
Psychological stress-induced cerebrovascular dysfunction: the role of metabolic syndrome and exercise.
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DOI：
10.1113/ep086892
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发表时间：
2018-05-01
影响因子：
2.7
通讯作者：
Chantler PD
中科院分区：
文献类型：
--
作者：
Brooks S;Branyan KW;DeVallance E;Skinner R;Lemaster K;Sheets JW;Pitzer CR;Asano S;Bryner RW;Olfert IM;Frisbee JC;Chantler PD
长期无法解决的压力导致抑郁症和心血管疾病（CVD）的发展。代谢综合征（MetS）伴发抑郁症的患病率较高，但MetS伴发心理应激对脑血管功能的影响程度尚不清楚。我们研究了MetS对大鼠（16-17周龄）在8周不可预测的慢性轻度应激（UCMS）后脑血管结构/功能的不同影响，以及运动训练是否可以限制任何脑血管功能障碍。在健康瘦大鼠（LZR）中，UCMS使离体大脑中动脉（MCA）内皮依赖性舒张功能（EDD）降低（28%，p<0.05），但MCA重塑和僵硬度变化不明显，但脑微血管密度降低（MVD; 30%，p<0.05）。UCMS和MetS（OZR;肥胖Zucker大鼠）的存在降低了MCA EDD（35%，p<0.05）和硝普钠扩张（20%，p<0.05），而MCA硬度增加，脑MVD降低（31%，p<0.05），这与一氧化氮减少和氧化水平增加有关。有氧运动可预防LZR组UCMS对MCA功能和MVD的损害，而OZR组MCA功能、僵硬度和MVD可部分恢复。我们的数据表明，UCMS运动的好处是由于减少氧化应激，增加脑血管中一氧化氮的产生。总之，UCMS显着损害MCA的结构和功能，但UCMS对OZR的影响比LZR更显着。重要的是，有氧运动与UCMS相结合时，通过脑微血管中一氧化氮和氧化应激的微妙变化预防了MCA功能障碍。
Chronic unresolvable stress leads to the development of depression and cardiovascular disease (CVD). There is a high prevalence of depression with the metabolic syndrome (MetS), however, to what extent the MetS concurrent with psychological stress affects cerebrovascular function is unknown. We investigated the differential effect of MetS on cerebrovascular structure/function in rats (16–17-wk-old) following 8 wk of unpredictable chronic mild stress (UCMS), and whether exercise training could limit any cerebrovascular dysfunction. In healthy lean rats (LZR), UCMS decreased (28%, p<0.05) ex-vivo middle cerebral artery (MCA) endothelium-dependent dilation (EDD), however, changes in MCA remodeling and stiffness were not evident but cerebral microvessel density decreased (MVD; 30%, p<0.05). The presence of UCMS and MetS (OZR; obese Zucker rats) decreased MCA EDD (35%, p<0.05), and dilation to sodium nitroprusside (20%, p<0.05), while MCA stiffness increased, and cerebral MVD decreased (31%, p<0.05), which were linked to a reduced nitric oxide and increased oxidative levels. Aerobic exercise prevented UCMS impairments in MCA function and MVD in LZR, and partly restored MCA function, stiffness and MVD in OZR. Our data suggests that the benefits of exercise with UCMS was due to a reduction in oxidative stress, and increased production of nitric oxide in the cerebral vessels. In conclusion, UCMS significantly impaired MCA structure and function, but the effects of UCMS were more substantial in OZR vs. LZR. Importantly, aerobic exercise when combined with UCMS prevented the MCA dysfunction through subtle shifts in nitric oxide and oxidative stress in the cerebral microvasculature.