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.