Lambert Elisabeth, Hotchkin Elodie, Alvarenga Marlies, Pier Ciaran, Richards Jeffrey, Barton David, Dawood Tye, Esler Murray, Lambert Gavin
Human Neurotransmitter Laboratory, Baker Heart Research Institute, PO Box 6492 St Kilda Road Central, Melbourne, Victoria, Australia.
J Physiol. 2006 Feb 1;570(Pt 3):637-43. doi: 10.1113/jphysiol.2005.100040. Epub 2005 Nov 24.
Patients with panic disorder are at increased cardiac risk. While the mechanisms responsible remain unknown, activation of the sympathetic nervous system may be implicated. Using isotope dilution methodology, investigations of whole-body and regional sympathetic nervous activity have failed to show any differences between patients with panic disorder and healthy subjects. Using direct recording of single unit efferent sympathetic vasoconstrictor nerve activity by microneurography we examined sympathetic nervous function in patients with panic disorder more precisely than previously reported. The activity of multiunit and single unit vasoconstrictor sympathetic nerves was recorded at rest at the level of the peroneal nerve in 10 patients diagnosed with panic disorder and in nine matched healthy volunteers. Multiunit sympathetic activity was not different between the two groups (26+/-3 bursts min-1 in patients with panic disorder and 28+/-3 bursts min-1 in controls). The firing frequency of single unit vasoconstrictor neurones was also similar between the two groups (0.38+/-0.09 versus 0.22+/-0.03 Hz). However, the probability of firing during a sympathetic burst was higher in patients with panic disorder compared with healthy controls (45+/-5%versus 32+/-3%, P<0.05). When only the neural bursts during which the vasoconstrictor neurone was active were considered, we found that in patients with panic disorder the neurones tended to fire more often in a 'multiple spike' pattern than in the controls (i.e. the probability of the neurone firing twice was 25+/-3% in patients with panic disorder compared with 14+/-3% in controls). Quantification from single vasoconstrictor unit recording provides evidence of a disturbed sympathetic firing pattern in patients with panic disorder.
惊恐障碍患者的心脏风险增加。虽然其背后的机制尚不清楚,但交感神经系统的激活可能与之有关。采用同位素稀释法,对全身和局部交感神经活动的研究未能显示惊恐障碍患者与健康受试者之间存在任何差异。通过微神经ography直接记录单单位传出交感缩血管神经活动,我们比以前的报告更精确地检查了惊恐障碍患者的交感神经功能。在10例诊断为惊恐障碍的患者和9名匹配的健康志愿者中,在腓神经水平静息时记录多单位和单单位缩血管交感神经的活动。两组之间的多单位交感神经活动没有差异(惊恐障碍患者为26±3次爆发/分钟,对照组为28±3次爆发/分钟)。两组之间单单位缩血管神经元的放电频率也相似(分别为0.38±0.09Hz和0.22±0.03Hz)。然而,与健康对照组相比,惊恐障碍患者在交感神经爆发期间的放电概率更高(分别为45±5%和32±3%,P<0.05)。当仅考虑缩血管神经元活跃时的神经爆发时,我们发现惊恐障碍患者的神经元比对照组更倾向于以“多峰”模式更频繁地放电(即,惊恐障碍患者神经元放电两次的概率为25±3%,而对照组为14±3%)。从单缩血管单位记录进行量化提供了惊恐障碍患者交感神经放电模式紊乱的证据。