Abstract
Posttraumatic stress disorder (PTSD) causes mental and somatic diseases. Intermittent hypoxic conditioning (IHC) has cardio-, vaso-, and neuroprotective effects and alleviates experimental PTSD. IHC’s ability to alleviate harmful PTSD effects on rat heart, liver, and brain was examined. PTSD was induced by 10-day exposure to cat urine scent (PTSD rats). Some rats were then adapted to 14-day IHC (PTSD+IHC rats), while PTSD and untreated control rats were cage rested. PTSD rats had a higher anxiety index (AI, X-maze test), than control or PTSD+IHC rats. This higher AI was associated with reduced glycogen content and histological signs of metabolic and hypoxic damage and of impaired contractility. The livers of PTSD rats had reduced glycogen content. Liver and blood alanine and aspartate aminotransferase activities of PTSD rats were significantly increased. PTSD rats had increased norepinephrine concentration and decreased monoamine oxidase A activity in cerebral cortex. The PTSD-induced elevation of carbonylated proteins and lipid peroxidation products in these organs reflects oxidative stress, a known cause of organ pathology. IHC alleviated PTSD-induced metabolic and structural injury and reduced oxidative stress. Therefore, IHC is a promising preventive treatment for PTSD-related morphological and functional damage to organs, due, in part, to IHC’s reduction of oxidative stress.
Highlights
Posttraumatic stress disorder (PTSD) is a condition caused by severe stress and subsequent chronic distress, which is generally associated with a life-threatening experience, such as a natural disaster, military combat, traffic accidents, incurable disease or a personal tragedy
Experimental PTSD increased the time spent in the closed arms of the elevated X-maize (Table 1) by 8.4% compared to the control group (p < 0.001), while intermittent hypoxia conditioning (IHC) alone reduced this time by 10% (p < 0.001)
For the PTSD+IHC group, the time spent in the closed arms was 11% shorter than for the PTSD group (p < 0.001), and this time did not significantly differ from that of the control group
Summary
Posttraumatic stress disorder (PTSD) is a condition caused by severe stress and subsequent chronic distress, which is generally associated with a life-threatening experience, such as a natural disaster, military combat, traffic accidents, incurable disease or a personal tragedy. Incidence of PTSD is increasing, approximately 60–80% of humans and animals exposed to severe stress do not develop PTSD [5,6,7]. This individual resistance to PTSD is apparently based on genetically determined potency of endogenous defense systems called stress-limiting systems, which include heat shock proteins (HSPs), antioxidants, nitric oxide, prostaglandins, and serotonergic, GABAergic and other systems [8,9,10]. IHC preconditioning [16] and postconditioning [17] were shown to abolish development of stress-induced anxiety in the rat “stress-restress” model of PTSD. IHC exerted a robust anti-stress effect in naïve rats, as evidenced from less anxiety during an elevated X-maze test [18]
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