Altitude hypoxia effects on brain.

Abstract

Hypoxic cerebral vasodilation is mediated by a complex pathway through glial cells positioned between neurones and cerebral artenoles, and involving both K and adenosine release into ECF. Lactic acidosis is of less importance than had been assumed. During the first hours at altitude, CBF rises 30-60% and then after some days, falls to nearly normal values. The magnitude ofthis transient rise depends on the altitude and the individual cerebral vascular and ventilatorz sensitivities to both O₂ and CO₂ The subsequent reduction of flow remains poorly understood, but is at least partly explained by rises of PaO₂, CSF pH, and fall of PaCO₂, but neither by polycythemia, nor reduced sensitivity of cerebral vessels to hypoxia Later effects of hypoxia include reduced blood and CSF buffer base increasing peripheral chemo receptor sensitivity, rising Hct and perhaps macrophage expression of VEGF None of the known factorsregulating C'BF (including polycythemia) can fully acount for the evidence that in several studies, natives of high altitude, and those fully acclimatized, have been found to have normal or subnormal CBF (compared with sea level normals) Reduced brain CMRO₂ has been reported in humans native to high altitude, which could help explain the low CBF AMS and HACE may be accompanied by high CBF, because PaO₂ is lower. but AMS and HACE cannot be caused by high CBF since hypercapnia fails to cause symptomatic illness, despite higher flow Subtle brain injury seen in mountaineers may be related to hypocapnic vasoconstriction and a marked alkaline Bohr downshift in capillary PO₂ Capillary inJury at high altitude may result from the cytokine VEGF released in hypoxic brain by macrophages initiating angiogenesis.