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抑郁和非抑郁个体在停止哭泣时的迷走神经反弹。

Vagal rebound during resolution of tearful crying among depressed and nondepressed individuals.

作者信息

Rottenberg Jonathan, Wilhelm Frank H, Gross James J, Gotlib Ian H

机构信息

Mood and Anxiety Disorders Laboratory, Department of Psychology, Stanford University, Stanford, California 94305-2130, USA.

出版信息

Psychophysiology. 2003 Jan;40(1):1-6. doi: 10.1111/1469-8986.00001.

Abstract

Respiratory sinus arrhythmia (RSA) is an index of the vagal control of heart rate that is associated with emotion regulatory capacity. To examine RSA in depressed and nondepressed participants in the context of an emotion-regulatory challenge, we presented a sad film to induce crying, a behavior associated with heightened parasympathetic activation. We predicted that nondepressed persons who cried would show elevations in RSA during the onset and the resolution of crying. By contrast, we predicted that depressed individuals who cried would fail to exhibit increased RSA over the course of their crying episodes. As hypothesized, nondepressed participants exhibited RSA increases that accompanied the resolution of tearful crying, consistent with a homeostatic function for crying, whereas depressed subjects who cried did not exhibit increased RSA. Results suggest that the physiological self-regulatory mechanisms invoked by crying are compromised in depression.

摘要

呼吸性窦性心律不齐(RSA)是一种与情绪调节能力相关的迷走神经对心率控制的指标。为了在情绪调节挑战的背景下检查抑郁和非抑郁参与者的RSA,我们播放了一部悲伤的电影以诱发哭泣,哭泣是一种与副交感神经激活增强相关的行为。我们预测,哭泣的非抑郁者在哭泣开始和结束时RSA会升高。相比之下,我们预测哭泣的抑郁个体在哭泣过程中不会表现出RSA增加。正如假设的那样,非抑郁参与者在含泪哭泣结束时表现出RSA增加,这与哭泣的稳态功能一致,而哭泣的抑郁受试者没有表现出RSA增加。结果表明,哭泣所引发的生理自我调节机制在抑郁症中受到损害。

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