Basic physiology and energy metabolism of the central nervous
system
Despite the fact that only 2% of our total body weight constitutes of
brain tissue, its metabolic demands are high. Nearly 20% of the total
oxygen and 20% of the glucose consumption is utilized by our central
nervous tissue. Most of the oxygen and glucose consumption is used to
maintain the membrane potential through Na +/ K+ -ATPase and other processes involved in ion
transport across membranes. The brain energy source does not come from
fatty acids but is almost exclusively based on saccharide sources with a
daily consumption of glucose of about 120 g. The interplay between
neurons and astrocytes is particularly important in the energy
metabolism of the brain: astrocytes are primarily anaerobic in terms of
ATP generation via anaerobic glycolysis and net lactate extrusion while
neurons primarily have a high level of aerobic mitochondrial metabolism
(1). Astrocytes, specialized glial cells metabolically supporting the
neurons and outnumbering neurons by fivefold, mainly consume glucose
while neurons rely primarily on lactate and pyruvate, substances
released by astrocytes into the extracellular space and absorbed into
the neurons. The higher the activity of the neuron, the higher the
production of lactate in the astrocyte. Glutamate, the most important
neurotransmitter within the central nervous system, is transported from
the synaptic cleft into the astrocytes. These cells reform glutamate
into glutamine and return it back to the neuron for further utilization.
On the other hand is our brain very sensitive to deficits of oxygen and
glucose. Even after a few seconds a shortage of oxygen may cause
unconsciousness and after about 5 minutes irreversible neuronal damage
may occur at normothermia. This low sensitivity to hypoxia is evident by
the well-known capability to culture astrocytes for up to 24 hours from
adult brain tissue whereas neurons survive less than 5 minutes in an
anoxic environment (1).
In healthy adults the cerebral autoregulation keeps the cerebral blood
flow constant throughout a range of perfusion pressures between 50 and
150 mm Hg (2). These limits decrease to 30 and 100 mm Hg at 22° C brain
temperature but at lower temperatures autoregulation is terminated and
cerebral blood flow becomes directly proportional to cerebral perfusion
pressure (3).
Related to aortic arch surgery causes of neurologic complications are
either thromboembolic (atheroma, debris, air) leading to focal defects
or interruption of the normal cerebral perfusion with insufficient
cerebral protection leading to more global injuries. Both these
mechanisms of injury need to be tackled during arch repair. In acute
dissection patients atherosclerosis is mostly absent. No need to say
that transient and/or permanent neurological deficits will have a
negative impact on short- and long-term survival.