Woods S W, Charney D S, Loke J, Goodman W K, Redmond D E, Heninger G R
Arch Gen Psychiatry. 1986 Sep;43(9):900-9. doi: 10.1001/archpsyc.1986.01800090090013.
One hypothesis that could account for the anxiogenic response to breathing air supplemented with carbon dioxide seen in panic anxiety patients is that panic patients might have abnormally high central medullary chemoreceptor sensitivity. Chemoreceptor sensitivity was assessed by using a rebreathing technique to measure the ventilatory response to CO2 in 14 medication-free patients with agoraphobia and panic attacks and 23 healthy subjects. Ventilatory response to CO2 was similar in patients and controls (mean +/- SEM, 1.58 +/- 0.16 vs 1.58 +/- 0.14 L/min/mm Hg), suggesting that abnormal chemoreceptor sensitivity does not explain the behavioral sensitivity of panic patients to CO2. Anxiety ratings increased markedly during rebreathing both in patients and controls; anxiety increases were significantly greater in patients than in healthy subjects matched for age, sex, and rebreathing duration. Alprazolam treatment in eight patients markedly attenuated anxiety increases during rebreathing. Differences in anxiogenic sensitivity to CO2 between patients and controls may be due to differences in the regulation of noradrenergic or other neuronal systems.
一种可以解释惊恐障碍患者在呼吸补充二氧化碳的空气时产生焦虑反应的假说认为，惊恐障碍患者可能具有异常高的中枢髓质化学感受器敏感性。通过使用重复呼吸技术测量14名未服用药物的广场恐惧症和惊恐发作患者以及23名健康受试者对二氧化碳的通气反应来评估化学感受器敏感性。患者和对照组对二氧化碳的通气反应相似（平均值±标准误，1.58±0.16对1.58±0.14升/分钟/毫米汞柱），这表明化学感受器敏感性异常并不能解释惊恐障碍患者对二氧化碳的行为敏感性。患者和对照组在重复呼吸过程中焦虑评分均显著增加；患者的焦虑增加显著大于年龄、性别和重复呼吸持续时间相匹配的健康受试者。8名患者接受阿普唑仑治疗后，重复呼吸过程中焦虑增加明显减轻。患者和对照组之间对二氧化碳焦虑敏感性的差异可能归因于去甲肾上腺素能或其他神经元系统调节的差异。
