Fig. 3.

Proposed mechanisms underlying development of AH. Berilgen et al. [7] suggest that AH results from local inflammation caused by sinus barotrauma due to changes in the atmospheric pressure during the landing. The first degree of sinus barotrauma [41] is a short lasting discomfort with almost no anatomical changes in the sinuses and can be considered as a potential player in AH. Most passengers sense pressure changes during landing and gas trapping in the sinuses often occurs that can contribute in sinus barotrauma and a transient local inflammation. Since we identified that PGE₂, an inflammation mediator, was higher in AH-group and SPO was lower, we suggest that a mild hypoxia may occur during a flight travel that may lead to reflective but perhaps mild hyperventilation. Hyperventilation can result in decreasing levels of carbon dioxide (CO₂) and elevated blood pH [42]. As a response to the decreased CO₂, vasodilation may occur [42]. Vasodilation in the cerebral arteries as a reaction to local inflammation or hypoxia can theoretically lead to development of AH. This hypothesis should be examined. Furthermore, interrelationship between anxiety, stress and other environmental and internal subjective factors linked with AH should also be investigated thoroughly to approve or falsify the theoretical model presented here