Altered Autoregulation Of Cerebral Blood Flow In Hypoxia: Relevance To The Pathophysiology Of Acute Mountain Sickness
Acute mountain sickness (AMS) is a syndrome of headache, anorexia, nausea and fatigue, which commonly occurs with rapid ascent to high altitudes. The pathogenesis of AMS remains incompletely understood. A leading theory has been that AMS could be an early stage manifestation of high altitude cerebral edema, which sometimes complicates AMS and is of poor prognosis. There has indeed been recent reports of magnetic resonance imaging (MRI) evidence of hypoxia-induced reversible brain edema in healthy volunteers. Interestingly, in these studies, brain edema was both vasogenic and cytotoxic but with only the MRI cytotoxicity signals correlated to AMS symptomatology. Studies in volunteers exposed to normobaric or hypobaric hypoxic conditions have disclosed a hypoxia-induced alteration of the autoregulation of cerebral blood flow in proportion to the severity of oxygen deprivation and to AMS symptoms. The alteration of cerebral autoregulation contributes to breathing instability during sleep and may thereby promote periodic breathing and nocturnal oxygen desaturation. The alteration of cerebral autoregulation could also be a cause of overperfusion of cerebral capillaries and vasogenic edema during exercise and/or cold exposure. A common cause for altered cerebral autoregulation and cytotoxic brain edema could be hypoxia-induced release of oxygen free radicals. Thus, AMS is likely the result of a dynamic interaction between hemodynamic and cytotoxic events.
Keywords: Altitude; brain; cerebral blood flow; acute mountain sickness; cerebral edema
KeywordsPlacebo Fatigue Dioxide Magnesium Filtration
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