Modulation of pain-induced endothelial dysfunction by hypnotisability

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.