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重度抑郁症期间及疾病缓解后脑血管反应性的评估。

Assessment of cerebrovascular reactivity during major depression and after remission of disease.

作者信息

Vakilian Alireza, Iranmanesh Farhad

机构信息

Department of Neurology, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.

出版信息

Ann Indian Acad Neurol. 2010 Jan;13(1):52-6. doi: 10.4103/0972-2327.61278.

DOI:10.4103/0972-2327.61278
PMID:20436748
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2859589/
Abstract

BACKGROUND

There are a growing number of studies suggesting that depression may increase the risk of stroke. Impaired autoregulation of vascular tone may contribute to a higher risk of developing cerebrovascular diseases. Cerebrovascular reactivity (CVR) reflects the compensatory dilatory capacity of cerebral arterioles to a dilatory stimulus and is an important mechanism that ensures constant cerebral blood flow. There is a hypothesis that CVR is reduced in major depression, which would explain the association between depression and stroke.

OBJECTIVES

The aim of this study was to investigate the effect of depression on CVR in cerebral vessels by comparing CVR during the depression phase with that during remission.

MATERIAL AND METHODS

Using the apnea test, we assessed CVR in 16 patients with unipolar depression during disease and after remission of disease by calculating the increase in cerebral blood flow velocity after breath-holding (the apnea test). Blood flow velocities were measured by transcranial Doppler ultrasound (TCD).

RESULTS

CVR was significantly reduced in the depression phase in comparison to that in the remission phase. However, this change was not seen in all the patients.

CONCLUSION

CVR was reduced in most of the depressed patients. The decreased CVR, as indicated by the changes in peak systolic velocity (PSV) and mean flow velocity (MFV) of the middle cerebral artery, in depressed patients was more marked on the right side, which could point to a vascular basis for some kinds of depression. We recommend that other studies, with larger samples, be done; future studies should assess whether the changes in the CVR varies with the severity and type of depression.

摘要

背景

越来越多的研究表明,抑郁症可能会增加中风风险。血管张力的自动调节受损可能会导致患脑血管疾病的风险更高。脑血管反应性(CVR)反映了脑小动脉对扩张刺激的代偿性扩张能力,是确保脑血流量恒定的重要机制。有一种假说认为,重度抑郁症患者的CVR会降低,这可以解释抑郁症与中风之间的关联。

目的

本研究的目的是通过比较抑郁症发作期和缓解期的CVR,来研究抑郁症对脑血管CVR的影响。

材料与方法

我们采用屏气试验,通过计算屏气后(屏气试验)脑血流速度的增加,评估了16例单相抑郁症患者在患病期间和疾病缓解后的CVR。血流速度通过经颅多普勒超声(TCD)测量。

结果

与缓解期相比,抑郁症发作期的CVR显著降低。然而,并非所有患者都出现这种变化。

结论

大多数抑郁症患者的CVR降低。抑郁症患者中,如大脑中动脉收缩期峰值速度(PSV)和平均流速(MFV)的变化所示,CVR降低在右侧更为明显,这可能为某些类型的抑郁症提供血管基础。我们建议开展其他更大样本量的研究;未来的研究应评估CVR的变化是否随抑郁症的严重程度和类型而变化。

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引用本文的文献

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Front Psychiatry. 2019 May 31;10:373. doi: 10.3389/fpsyt.2019.00373. eCollection 2019.
2
Comparison of CO2 in air versus carbogen for the measurement of cerebrovascular reactivity with magnetic resonance imaging.空气与碳化氧合作用(carbogen)在磁共振成像测量脑血管反应性方面的 CO2 比较。
J Cereb Blood Flow Metab. 2013 Nov;33(11):1799-805. doi: 10.1038/jcbfm.2013.131. Epub 2013 Aug 7.

本文引用的文献

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[Depression as the cause and consequence of cerebrovascular diseases].[抑郁症作为脑血管疾病的病因及后果]
Med Pregl. 2007 May-Jun;60(5-6):255-60. doi: 10.2298/mpns0706255r.
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Cerebrovascular reactivity in depressed patients without vascular risk factors.无血管危险因素的抑郁症患者的脑血管反应性
J Psychiatr Res. 2008 Jan;42(1):78-82. doi: 10.1016/j.jpsychires.2006.10.001. Epub 2006 Nov 20.
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Cerebrovascular reactivity over time course in healthy subjects.健康受试者脑血管反应性随时间的变化过程。
J Neurol Sci. 2006 Nov 15;249(2):135-9. doi: 10.1016/j.jns.2006.06.009. Epub 2006 Jul 21.
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Cerebrovascular reactivity in major depression: a pilot study.重度抑郁症中的脑血管反应性:一项初步研究。
Psychosom Med. 2004 Jan-Feb;66(1):6-8. doi: 10.1097/01.psy.0000107880.03026.54.
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Stroke. 2001 Apr;32(4):903-8. doi: 10.1161/01.str.32.4.903.
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Symptoms of depression as a prospective risk factor for stroke.抑郁症症状作为中风的一个前瞻性风险因素。
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Impaired cerebrovascular reactivity as a risk marker for first-ever lacunar infarction: A case-control study.脑血管反应性受损作为首次腔隙性脑梗死的风险标志物:一项病例对照研究。
Stroke. 1999 Nov;30(11):2296-301. doi: 10.1161/01.str.30.11.2296.
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Fluoxetine dilates isolated small cerebral arteries of rats and attenuates constrictions to serotonin, norepinephrine, and a voltage-dependent Ca(2+) channel opener.氟西汀可扩张大鼠离体的大脑小动脉,并减弱对5-羟色胺、去甲肾上腺素和一种电压依赖性Ca(2+)通道开放剂的收缩反应。
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