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运动期间大脑氧合与中年高血压和正常血压个体靶器官损伤的关系。

Association of Cerebral Oxygenation During Exercise With Target Organ Damage in Middle-Aged Hypertensive and Normotensive Individuals.

机构信息

3rd Department of Internal Medicine, Papageorgiou General Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece.

Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA.

出版信息

Am J Hypertens. 2022 Jul 1;35(7):664-671. doi: 10.1093/ajh/hpac040.

DOI:10.1093/ajh/hpac040
PMID:35325928
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11024639/
Abstract

BACKGROUND

The brain is one of the main target organs affected by hypertension. Impaired cerebral oxygenation during exercise is an indicator of cerebral dysfunction. We aimed to investigate whether cerebral oxygenation during exercise correlates with subclinical markers of early target organ damage in a population of middle-aged, newly diagnosed hypertensive and healthy individuals.

METHODS

Carotid intima-media thickness (cIMT) was measured using ultrasound, arterial stiffness was estimated measuring the augmentation index and pulse wave velocity, and retinal vessel diameter was assessed via the central retinal-arteriolar and vein equivalent and retinal-arteriovenous ratio. Participants (n = 93) performed a 3-minute isometric handgrip exercise. Cerebral prefrontal oxygenation was measured continuously using near infrared spectroscopy. The average exercise responses in oxygenated hemoglobin (O2Hb), deoxygenated hemoglobin (HHb), and total hemoglobin (tHb) were assessed. Univariate analyses were performed; partial correlation was used to account for traditional cardiovascular risk factors to identify independent associations between cerebral-oxygenation indices and early markers of target organ damage.

RESULTS

Mean cIMT was negatively correlated with the average exercise response in cerebral oxygenation (rhoO2Hb = -0.348, PO2Hb = 0.001; rhotHb = -0.253, Pthb = 0.02). Augmentation index was negatively correlated with cerebral oxygenation during exercise (rhoO2Hb = -0.374, P < 0.001; rhotHb = -0.332, P = 0.02), whereas no significant correlation was observed between pulse wave velocity and cerebral-oxygenation indices. In the adjusted analysis, cerebral oxygenation was correlated with central retinal arteriolar diameter (CRAE r = 0.233, P = 0.043).

CONCLUSIONS

Our novel findings suggest that indices of lower cerebral oxygenation during a submaximal physical task are associated with markers of early, subclinical target organ damage, namely increased cIMT, arterial stiffness, and arteriolar retinal narrowing in newly diagnosed, untreated, hypertensive individuals.

摘要

背景

大脑是受高血压影响的主要靶器官之一。运动期间脑氧合受损是脑功能障碍的一个指标。我们旨在研究在中年新诊断高血压和健康人群中,运动期间的脑氧合是否与早期靶器官损伤的亚临床标志物相关。

方法

使用超声测量颈动脉内膜中层厚度(cIMT),通过测量增强指数和脉搏波速度来估计动脉僵硬度,并通过中央视网膜动脉等效直径和视网膜动静脉比评估视网膜血管直径。参与者(n = 93)进行了 3 分钟的等长握力运动。使用近红外光谱连续测量前额叶的脑氧合。评估了氧合血红蛋白(O2Hb)、去氧血红蛋白(HHb)和总血红蛋白(tHb)的平均运动反应。进行了单变量分析;使用偏相关来解释传统心血管危险因素,以确定脑氧合指数与靶器官早期损伤标志物之间的独立关联。

结果

平均 cIMT 与脑氧合的平均运动反应呈负相关(rhoO2Hb = -0.348,PO2Hb = 0.001;rhotHb = -0.253,Pthb = 0.02)。增强指数与运动期间的脑氧合呈负相关(rhoO2Hb = -0.374,P < 0.001;rhotHb = -0.332,P = 0.02),而脉搏波速度与脑氧合指数之间无显著相关性。在调整分析中,脑氧合与中央视网膜小动脉直径(CRAE r = 0.233,P = 0.043)相关。

结论

我们的新发现表明,亚最大体力活动期间较低的脑氧合指数与早期亚临床靶器官损伤的标志物相关,即新诊断、未经治疗的高血压个体中 cIMT 增加、动脉僵硬度和小动脉视网膜变窄。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27b0/11024639/081e3dec4e39/hpac040_fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27b0/11024639/a4e877c2649c/hpac040_fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27b0/11024639/ffea5dad45b3/hpac040_fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27b0/11024639/8fae3e4dd80a/hpac040_fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27b0/11024639/095a41706518/hpac040_fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27b0/11024639/081e3dec4e39/hpac040_fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27b0/11024639/a4e877c2649c/hpac040_fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27b0/11024639/ffea5dad45b3/hpac040_fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27b0/11024639/8fae3e4dd80a/hpac040_fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27b0/11024639/095a41706518/hpac040_fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27b0/11024639/081e3dec4e39/hpac040_fig4.jpg

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