Jambrik Zoltan, Santarcangelo Enrica L, Rudisch Tibor, Varga Albert, Forster Tamas, Carli Giancarlo
II Department of Internal Medicine and Cardiology Centre, University of Sciences, Szeged, Hungary Department of Physiology and Biochemistry, Pisa University, Italy Department of Neuropsychology Rehabilitation, Szeged University, Hungary Department of Physiology, University of Siena, Via A. Moro, 4 Siena, Italy.
Pain. 2005 Aug;116(3):181-186. doi: 10.1016/j.pain.2005.03.041.
Mental stress induces endothelial dysfunction, that is a reduction of the post-occlusion brachial artery flow-mediated vasodilation (FMD). This does not occur in subjects highly susceptible to hypnosis (Highs) in either the waking or hypnotic state. The aim of the present experiment was to assess whether endothelial dysfunction is also induced by acute nociceptive stimulation and whether high hypnotisability and/or the specific instruction of analgesia prevent its occurrence in awake highly hypnotizable individuals. Thus, nine Highs and nine subjects with low susceptibility to hypnosis (Lows) underwent an experimental session including the administration of pressor pain and of pressor pain associated with the instruction of analgesia. Heart rate, basal artery diameters and brachial artery flow-mediated vasodilation were measured during stimulation and rest conditions. Heart rate exhibited slight changes not modulated by hypnotisability. During painful stimulation both Highs and Lows showed a decrease of FMD, but it was significantly less pronounced in Highs. During the administration of painful stimulation together with the instruction of analgesia, only Highs reported analgesia and their FMD no longer decreased. This study provides the first evidence of pain-related endothelial dysfunction and extends previous findings concerning a sort of natural protection of Highs against the vascular effects of mental stress to acute pain.
精神压力会导致内皮功能障碍，即肱动脉闭塞后血流介导的血管舒张（FMD）降低。无论是在清醒状态还是催眠状态下，这种情况在高度易受催眠的受试者（Highs）中都不会发生。本实验的目的是评估急性伤害性刺激是否也会导致内皮功能障碍，以及高催眠易感性和/或特定的镇痛指令是否能防止其在清醒的高催眠易感性个体中发生。因此，9名Highs和9名低催眠易感性受试者（Lows）接受了一个实验环节，包括施加升压性疼痛以及与镇痛指令相关的升压性疼痛。在刺激和休息状态下测量心率、基础动脉直径和肱动脉血流介导的血管舒张。心率表现出轻微变化，不受催眠易感性的调节。在疼痛刺激期间，Highs和Lows的FMD均下降，但Highs的下降明显不那么明显。在施加疼痛刺激并给予镇痛指令时，只有Highs报告有镇痛效果，且他们的FMD不再下降。本研究首次提供了与疼痛相关的内皮功能障碍的证据，并将先前关于Highs对精神压力的血管效应具有某种天然保护作用的研究结果扩展到急性疼痛。
