The effects of ischemia and hypoxia

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Due to the high energy demand of CNS neurons oxygen it needs significant maintenance. Neuron cortex consumes 250-450 l O2 / min (for comparison - gliacyte hepatocyte and consume up to 60 l O2). Reduction of brain oxygen consumption is only 20% may cause loss of consciousness in humans. The disappearance of the impulse activity of neurons occurs in the first ten seconds of cerebral ischemia. After 5-6 minutes after the start of asphyxiation comes profound and often irreversible damage of brain activity. Neuronal loss in ischemia is the result of complex interconnected intracellular processes.

When cerebral anoxia primarily affected cortex. The death of the whole brain is "brain death", which appears in the complete disappearance of the bioelectric activity. Phylogenetically older structures of the central nervous system (spinal cord, brain stem) are less sensitive to asphyxia than younger (subcortex and especially the bark). Therefore decortication may occur if belated revival of the organism.

It is very sensitive to anoxia brakes. One consequence of this is a disinhibition of CNS structures intact. In the early stages of ischemic brain neurons when still capable of giving a reaction, they can hyperactivity. In the later stages of ischemia hyperactivation of neuronal changes to their inactivation.

With the arrival of Na + into the neuron is connected first, acute phase of injury neuron. The increase in Na + concentration in the cytosol of the neuron leads to increased osmolarity, which causes the water input into the neuron and its swelling. Further increasing the osmolarity of the neuron it is also associated with the accumulation of Ca2 + in it, lactic acid, inorganic phosphorus. Since Ca2 + entry in the second phase is associated neuron neuron damage. Increasing the amount of Ca2 + entering the neuron is determined by the activation of glutamate receptors due to enhanced release of glutamate in nerve endings during ischemia. Antagonists of glutamate receptors and Ca2 + antagonists (blockers of Ca2 + channels) capable of preventing ischemic neuronal degeneration and to provide a therapeutic effect.

Neuron damage occurs not only during ischemia, but also in connection with renewal of cerebral reperfusion and the blood circulation. They may be the main danger. A major role in the post-ischemic reperfusion injury play: a new wave revenues Ca2 + into the neuron, POL (lipid peroxidation), and the processes of free radical oxidation, enhanced due to the influence of the incoming oxygen. Increased content of lactic acid due to receipt of glucose in violation of the conditions of oxidative phosphorylation, and increased anaerobic glycolysis. There is a swelling of the brain due to water inflow from the blood circulation at the resumption.

The complex set of intracellular Ca2 + - inducible damage include: alteration of intracellular proteins, increased phospholipase hydrolysis and proteolysis, the destruction of intracellular structures, damage to the cytoplasmic and intracellular membranes, swelling of neurons, violation of genome activity. On a critical increase in the intensity of these processes irreversible damage and death of a neuron, a so-called calcium death.

In the later stages of the pathological process caused by cerebral ischemia, as well as chronic process, a new set of secondary changes -. Degenerative-dystrophic processes, violation of enzyme and metabolic systems, vascular changes, the formation of antibodies to brain tissue, autoimmune aggression, etc. They constitute the pathogenetic structure post-ischemic encephalopathy, which can continue to develop (a progressive development). These processes, as well as changes in other systems and organs with their consequences occur after the resuscitation of the body, especially if it has been a long and late. Taken together, they constitute a pathogenetic structure postresuscitative disease (VA Negovsky).

Hypoxia varying degrees accompanied by many (if not all) forms of brain pathology. As a standard and non-specific process, it may, however, make a significant contribution to its development. However, moderate hypoxia can stimulate the metabolic and plastic processes in the neuron, to promote the adaptation and increase resistance, increase the trophic and plastic potential of the neuron, to enhance the adaptive capacity of the brain