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惊恐障碍患者在静息状态、实验室心理应激期间及惊恐发作时的交感神经活动。

Sympathetic activity in patients with panic disorder at rest, under laboratory mental stress, and during panic attacks.

作者信息

Wilkinson D J, Thompson J M, Lambert G W, Jennings G L, Schwarz R G, Jefferys D, Turner A G, Esler M D

机构信息

Human Neurotransmitter Research Laboratory, Baker Medical Research Institute, and the Alfred Heart Centre, Prahran, Melbourne, Australia.

出版信息

Arch Gen Psychiatry. 1998 Jun;55(6):511-20. doi: 10.1001/archpsyc.55.6.511.

Abstract

BACKGROUND

The sympathetic nervous system has long been believed to be involved in the pathogenesis of panic disorder, but studies to date, most using peripheral venous catecholamine measurements, have yielded conflicting and equivocal results. We tested sympathetic nervous function in patients with panic disorder by using more sensitive methods.

METHODS

Sympathetic nervous and adrenal medullary function was measured by using direct nerve recording (clinical microneurography) and whole-body and cardiac catecholamine kinetics in 13 patients with panic disorder as defined by the DSM-IV, and 14 healthy control subjects. Measurements were made at rest, during laboratory stress (forced mental arithmetic), and, for 4 patients, during panic attacks occurring spontaneously in the laboratory setting.

RESULTS

Muscle sympathetic activity, arterial plasma concentration of norepinephrine, and the total and cardiac norepinephrine spillover rates to plasma were similar in patients and control subjects at rest, as was whole-body epinephrine secretion. Epinephrine spillover from the heart was elevated in patients with panic disorder (P=.01). Responses to laboratory mental stress were almost identical in patient and control groups. During panic attacks, there were marked increases in epinephrine secretion and large increases in the sympathetic activity in muscle in 2 patients but smaller changes in the total norepinephrine spillover to plasma.

CONCLUSIONS

Whole-body and regional sympathetic nervous activity are not elevated at rest in patients with panic disorder. Epinephrine is released from the heart at rest in patients with panic disorder, possibly due to loading of cardiac neuronal stores by uptake from plasma during surges of epinephrine secretion in panic attacks. Contrary to popular belief, the sympathetic nervous system is not globally activated during panic attacks.

摘要

背景

长期以来,人们一直认为交感神经系统参与惊恐障碍的发病机制,但迄今为止的研究大多采用外周静脉儿茶酚胺测量,结果相互矛盾且不明确。我们使用更敏感的方法测试了惊恐障碍患者的交感神经功能。

方法

采用直接神经记录(临床微神经ography)以及全身和心脏儿茶酚胺动力学,对13例符合《精神疾病诊断与统计手册》第四版(DSM-IV)定义的惊恐障碍患者和14名健康对照者进行交感神经和肾上腺髓质功能测量。测量在静息状态、实验室应激(强迫心算)时进行,对4例患者还在实验室环境中自发惊恐发作时进行。

结果

静息时,患者和对照者的肌肉交感神经活动、动脉血浆去甲肾上腺素浓度、血浆总去甲肾上腺素溢出率和心脏去甲肾上腺素溢出率相似,全身肾上腺素分泌情况也相似。惊恐障碍患者心脏肾上腺素溢出增加(P = 0.01)。患者组和对照组对实验室精神应激的反应几乎相同。在惊恐发作期间,2例患者肾上腺素分泌显著增加,肌肉交感神经活动大幅增加,但血浆总去甲肾上腺素溢出变化较小。

结论

惊恐障碍患者静息时全身和局部交感神经活动并未升高。惊恐障碍患者静息时心脏释放肾上腺素,可能是由于在惊恐发作时肾上腺素分泌激增期间,血浆摄取使心脏神经元储存负荷增加所致。与普遍看法相反,惊恐发作期间交感神经系统并非全面激活。

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