Department of Psychiatry, Sacco Hospital, Milano 20157, Italy.
Psychoneuroendocrinology. 2013 Oct;38(10):2234-42. doi: 10.1016/j.psyneuen.2013.04.008. Epub 2013 May 20.
Neuroactive steroids modulate anxiety in experimental animals and possibly in humans. The secretion of these compounds has been found to be altered in panic disorder (PD), with such alterations having been suggested to be a possible cause or effect of panic symptomatology. Panic-like attacks can be induced in healthy individuals by administration of panicogenic agents or by physical procedures, and we have now measured the plasma concentrations of neuroactive steroids in such individuals before, during, and after panicogenic inhalation of CO2 in order to investigate whether abnormalities of neuroactive steroid secretion might contribute to the pathogenesis of PD. Fifty-nine psychologically and physically healthy subjects, including 42 women (11 in the follicular phase of the menstrual cycle, 14 in the luteal phase, and 17 taking contraceptive pills) and 17 men, who experienced a panic-like attack on previous exposure to 7% CO2 were again administered 7% CO2 for 20min. Thirty-three of these individuals (responders) again experienced a panic-like attack, whereas the remaining 26 subjects did not (nonresponders). All subjects were examined with the VAS-A and PSL-III-R scales for anxiety and panic symptomatology before and after CO2 inhalation. The plasma concentrations of progesterone, 3α,5α-tetrahydroprogesterone (3α,5α-THPROG=allopregnanolone), 3α,5α-tetrahydrodesoxycorticosterone (3α,5α-THDOC), dehydroepiandrosterone (DHEA), and cortisol were measured 15min and immediately before the onset of CO2 administration as well as immediately, 10, 30, and 50min after the end of CO2 inhalation. Neuroactive steroids were measured in the laboratory of Prof. Biggio in Cagliari, Sardinia, Italy. Neurosteroid levels did not change significantly in both responders and nonresponders before, during, or after CO2 inhalation. These data suggest that neuroactive steroid concentrations before, during, or after CO2 inhalation do not seem to correlate with panic symptomatology during panic-like attacks in subjects not affected by PD, and they therefore do not support the notion that abnormalities in neuroactive steroid secretion are either a cause or an effect of such attacks.
神经活性甾体可调节实验动物的焦虑，也可能调节人类的焦虑。已经发现，这些化合物的分泌在惊恐障碍（PD）中发生改变，这种改变被认为可能是惊恐症状的一个原因或结果。健康个体通过给予惊恐诱发剂或躯体程序可诱发类似惊恐的发作，我们目前已经测量了在惊恐样发作期间、之前和之后接受 CO2 吸入的个体的神经活性甾体的血浆浓度，以研究神经活性甾体分泌的异常是否可能促成 PD 的发病机制。59 名心理和躯体健康的个体，包括 42 名女性（11 名处于卵泡期，14 名处于黄体期，17 名服用避孕药）和 17 名男性，这些个体在以前暴露于 7%CO2 时经历过类似惊恐的发作，再次接受 20min 的 7%CO2 吸入。这些个体中有 33 名（有反应者）再次经历了类似惊恐的发作，而其余 26 名个体（无反应者）没有。所有个体在 CO2 吸入之前和之后均使用 VAS-A 和 PSL-III-R 量表评估焦虑和惊恐症状。在 CO2 给药前 15min 和即刻，以及 CO2 吸入结束后即刻、10min、30min 和 50min 时，测量了孕酮、3α,5α-四氢孕烯醇酮（3α,5α-THPROG=allopregnanolone）、3α,5α-四氢去氧皮质酮（3α,5α-THDOC）、脱氢表雄酮（DHEA）和皮质醇的血浆浓度。神经活性甾体的测量在意大利撒丁岛卡利亚里的比吉奥教授的实验室中进行。在有反应者和无反应者中，CO2 吸入之前、期间或之后，神经活性甾体水平均无显著变化。这些数据表明，在未受 PD 影响的个体中，在 CO2 吸入之前、期间或之后的神经活性甾体浓度与惊恐样发作期间的惊恐症状似乎没有相关性，因此，它们不支持神经活性甾体分泌异常是此类发作的原因或结果的观点。
