The Anxiolytic Effects of Moderate Hypoxia and Remote Ischemia in the Posttraumatic Stress Disorder Model Are Accompanied by Modification of Functioning of the Hypothalamic–Pituitary–Adrenal Axis

Abstract

Using a model of posttraumatic stress disorder (PTSD) in rats, it has been shown that conditioning by moderate hypobaric hypoxia (360 mmHg, three times for 2 h with 24-h interval) or limb ischemia–reperfusion (three times for 5 min with 15-min interval) prevents premature suppression of release of the stress hormone corticosterone to the blood plasma, which is typical of the triggering of pathological fast negative feedback of the hypothalamic–pituitary–adrenal axis (HPA) in this pathology. Hypoxic or remote ischemic preand postconditioning also increased the basal level of this hormone, which is significantly reduced during the formation of experimental PTSD. Thus, the pronounced anxiolytic effect of these conditioning types in the PTSD model may be mediated by the normalization of HPA regulation by a feedback mechanism and prevention of a decrease in its basal activity. Further research on the decoding of neurohumoral mechanisms of the stress-protective action of conditioning will speed up the introduction of these effective non-drug ways of prevention and correction of stress-induced pathologies into medical practice.