Seier F E, Kellner M, Yassouridis A, Heese R, Strian F, Wiedemann K
Department of Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany.
Am J Physiol. 1997 Jun;272(6 Pt 2):H2630-8. doi: 10.1152/ajpheart.1997.272.6.H2630.
To compare autonomic and neuroendocrine responses during lactate-induced panic attacks, heart rate variability and cortisol and atrial natriuretic hormone (ANH) levels were measured in patients with panic attacks and in healthy control subjects. In a randomized double-blind design, all subjects received either 10 ml/kg body weight of 0.5 M racemic sodium lactate or normal saline from 1100 to 1120. Spectral analysis of the R-R interval of analog electrocardiograms was performed, and total (0.001-0.45 Hz), low-frequency (0.01-0.05 Hz), midfrequency (0.05-0.15 Hz), and high-frequency power (0.15-0.45 Hz) were computed. Cortisol was measured 12 times in the period from 0900 to 1300, and ANH was measured at 1100, 1120, and 1200 by radioimmunoassay. In both panickers (n = 6) and nonpanickers (n = 8), an infusion of lactate resulted in an acceleration of heart rate, a reduction in total spectral power, and a decrease in the high- and low-frequency components of spectral power. Panickers showed a significant enhancement of the high-frequency power, whereas in nonpanickers, a shift from the mid- and high-frequency toward the low-frequency power emerged. ANH plasma concentrations during lactate infusion in panickers showed a significant increase (115 and 131% at 1120 and 1200, respectively, over concentrations at 1100) in contrast to nonpanickers (20 and 74%, respectively). No group or treatment effects on cortisol secretion emerged, which is in line with former reports. Our study supports preliminary observations that lactate-induced panic attacks enhance the release of ANH, a vasodilatator and inhibitor of sympathetic activity. Hence this hormone not only could inhibit the secretion of the stress hormone cortisol but, in parallel, could also attenuate the sympathetic stimulation to the heart. These inhibitory effects of ANH could explain the so-far-unresolved dissociation between psychopathological alterations and autonomic and endocrine responses of panic attacks.
为比较乳酸诱发惊恐发作期间的自主神经和神经内分泌反应，对惊恐发作患者和健康对照者测量了心率变异性、皮质醇和心房利钠激素（ANH）水平。在随机双盲设计中，所有受试者于11:00至11:20接受10ml/kg体重的0.5M消旋乳酸钠或生理盐水。对模拟心电图的R-R间期进行频谱分析，并计算总功率（0.001-0.45Hz）、低频功率（0.01-0.05Hz）、中频功率（0.05-0.15Hz）和高频功率（0.15-0.45Hz）。在09:00至13:00期间测量12次皮质醇，并在11:00、11:20和12:00通过放射免疫法测量ANH。在惊恐发作患者（n = 6）和非惊恐发作患者（n = 8）中，输注乳酸均导致心率加快、总频谱功率降低以及频谱功率的高频和低频成分减少。惊恐发作患者的高频功率显著增强，而非惊恐发作患者则出现从中频和高频功率向低频功率的转变。与非惊恐发作患者（分别为20%和74%）相比，惊恐发作患者在输注乳酸期间的ANH血浆浓度显著升高（11:20和12:00时分别比11:00时的浓度高115%和131%）。未发现对皮质醇分泌有组间或治疗效应，这与先前的报道一致。我们的研究支持了初步观察结果，即乳酸诱发的惊恐发作会增强血管舒张剂和交感神经活动抑制剂ANH的释放。因此，这种激素不仅可以抑制应激激素皮质醇的分泌，同时还可以减弱对心脏的交感神经刺激。ANH的这些抑制作用可以解释迄今为止惊恐发作的精神病理改变与自主神经和内分泌反应之间尚未解决的分离现象。
