Now hypobaric hypoxia, (Carlson et al., 2008). Microglial cell

Now
a day travelling to higher altitude and mountain climbing became a very
demanding and emerging subject in developing countries (Ref’s). At higher
altitude, there is decline in hypobaric pressure due to which partial pressure
of oxygen at that areas became lesser. It is like that altitude is inversely
proportional to the partial pressure of oxygen. The lack of availability of
oxygen at higher altitude due to decrease in partial pressure is well known as
hypobaric hypoxia (Ref’s). Hypobaric hypoxia is the major factor that leads to
many physiological manifestations in the people living at higher altitude or
migrate to higher altitude (Ref’s). So, dwellers and natives who are living at
higher altitude faced many of the problems like acute mountain sickness (AMS)
and chronic mountain sickness (CMS) (Ref’s) due to limited oxygen consumption
(Ref’s). To overcame to deficiency of oxygen in body, in tissue and blood,
their became modulation of many compensatory mechanism include activation of
carotid chemoreceptors (Ref’s), activation or formation of protein that leads
to gene transcription (Ref’s), stimulation of autonomic nervous system in order
to balance haemostasis by improving adequate blood supply (Ref’s), activation
of hypoxia inducible factor (HIF) (Ref’s), vascularization by vascular
endothelium growth factor (VEGF) (Ref’s), upregulation of Epo system to
increase oxygen carrying capacity by excessive erythrocytosis (Ref’s).

Brain, as it consumes a large amount of total oxygen at sea
level also, is highly susceptible to hypobaric hypoxia, (Carlson et al., 2008). Microglial cell are major immune cells
in the brain present in inactive state and highly sensitive to any cell damage
by chemical, physical or biological event (Ref’s). It is stated that the microglial
cells act as the innate immune in brain and constitute
the first line defence against tissue damage (Kreutzberg et al., 1996; Streit et al., 2005). During hypobaric hypoxic
condition, ATP crisis is assumed to be the main cause of ionic imbalance
mediated (calcium efflux) activation of several protease and phospholipase
(Ref’s). Further, protease and phospholipase are found to have role in the cell
necrosis and cell damage (Ref’s). Also, it is postulated that some of the
inflammatory mediators, including interleukins, cytokines, TNF-?, are released
in response to cell damage and responsible for several manifestations in
highlanders (Allen
and Orchard, 1987). Inflammatory
mediators are considered to facilitate microglial cells in dwellers at higher
altitude (Ref’s). Mitochondria is the main source of ATP and is vitally
responsible for haemostasis (Ref’s). The mitochondrial electron transport chain
(ETC), main source of ATP generation through oxidative phosphorylation, has
been found to blocked due to hypobaric hypoxia and assumed as one of the key
pathways of microglial activation by the help of reactive oxygen species (ROS)
(Ref’s). HIF activation is considered as the key compensatory mechanism in
response to hypobaric hypoxia and has found a great role in activation of
microglial cell through neuronal injury (Ref’s). Erythropoietin (Epo)
expression in patients with AMS as well as CMS assumed to play significant role
in acclimatization but it is also observed that Epo has a mechanistic role in
phosphorylation of Akt (Ref’s). Microglial activation in response to hypobaric
hypoxia is assumed mediate by Akt pathway (Ref’s). the peoples living at higher
altitude are suffering from many neurological disorders and microglial
activation has been reported to play significant role in the progression of
these neurological conditions (Ref’s). So, inhibition of microglial activation
may be the major target to improve many circumstances in dwellers at high
altitude.

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In this chapter,
we are exploring different possible mechanism of microglial activation in
response to hypobaric hypoxia.

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