The means by which it may be possible to protect the brain from ischemia are pharmacological or physical. Direct pharmacological interventions have focused on drugs that reduce the cerebral metabolic rate (and therefore reduce the demand for oxygen and energy substrate) and on agents that block the cellular mediators of ischemic injury (including calcium influx and the production of destructive protein kinases and free radicals). Physical means include the maintenance of an adequate cerebral perfusion pressure and arterial oxygen carriage and the optimizing of blood viscosity and temperature control.
With the exception of barbiturates , direct pharmacological brain protection has been, so far, disappointing. Traditionally, the dose of barbiturate is titrated to achieve burst suppression of the electroencephalogram (EEG). However, this has been questioned and there is evidence from animal studies that lower doses may be equally effective . Barbiturates depress the myocardium, dilate arterioles and interfere with normal baroreflexes and sympathetic tone, and may induce cardiovascular collapse in patients who are hypovolemic or have already impaired cardiovascular systems. Careful monitoring is essential and circulatory support may be required particularly in patients receiving higher doses. The intravenous anesthetic agent propofol may achieve a similar degree of protection with better cardiovascular stability .
There is evidence that mild hypothermia has a cerebral protective effect that exceeds that of the barbiturates and which is out of proportion to the degree to which the cerebral metabolic rate is lowered . Profound hypothermia during total circulatory arrest has been shown to be remarkably protective on gross measurement of outcome . Animal studies suggest that prolonged periods of arrest (>70 min) may be associated with damage to Purkinje's cells of the cerebellum ; however, the technique may allow procedures to be performed that would be otherwise impossible.
Hypothermia has a number of adverse effects, including poor wound healing, increased susceptibility to infection, alterations in platelet function, changes in drug metabolism and increased oxygen consumption during re-warming. However, with mild hypothermia (brain temperature of 34°C) the benefits seem to outweigh the risks.
Action to increase the mean arterial pressure whilst temporary vascular clips are in place during clipping of cerebral aneurysms is advocated by many authors. Some evidence exists for a beneficial effect of judiciously timed application of hyperbaric oxygen in focal and global ischemia, but the treatment may itself induce oxygen-free radical formation .
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