Woods S W, Charney D S, McPherson C A, Gradman A H, Heninger G R
Arch Gen Psychiatry. 1987 Apr;44(4):365-75. doi: 10.1001/archpsyc.1987.01800160077010.
To investigate the pathophysiology of nonpharmacologically induced panic attacks, 18 drug-free agoraphobic patients and 13 matched healthy subjects underwent structured exposure to phobic situations. Heart rate, blood pressure, and plasma free 3-methoxy-4-hydroxyphenylglycol (MHPG), cortisol, growth hormone, and prolactin levels were measured before, during, and after exposure. Fifteen patients experienced situational panic attacks during exposure. Panicking patients displayed significantly greater increases in heart rate but not blood pressure or plasma free MHPG or cortisol in comparison with the healthy subjects. Growth hormone and prolactin responses tended to be smaller in the patients. If brain noradrenergic hyperactivity occurs during situational panic attacks, it may be too brief or too restricted in regional localization to affect MHPG levels in plasma. Chronically recurrent attacks may cause an adaptation of neuroendocrine mechanisms activated by anxiety or stress.
为研究非药物诱导惊恐发作的病理生理学，18名未服用药物的广场恐怖症患者和13名匹配的健康受试者接受了针对恐惧情境的结构化暴露。在暴露前、暴露期间和暴露后测量心率、血压以及血浆游离3-甲氧基-4-羟基苯乙二醇（MHPG）、皮质醇、生长激素和催乳素水平。15名患者在暴露期间经历了情境性惊恐发作。与健康受试者相比，惊恐发作的患者心率显著增加，但血压、血浆游离MHPG或皮质醇未出现显著增加。患者的生长激素和催乳素反应往往较小。如果情境性惊恐发作期间发生脑去甲肾上腺素能功能亢进，其持续时间可能过短或在区域定位上过于局限，以至于无法影响血浆中的MHPG水平。慢性复发性发作可能会导致由焦虑或压力激活的神经内分泌机制产生适应性变化。
