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.
