Brain preservation

Damaging effects of an hypoxic or ischemic insult occur not only at the time of injury by dysfunction of neurotransmitters during the reflow period may initiate reactions that cause even more extensive tissue destruction. In addition, other preventable complications such as systemic hypotension, pulmonary hypoxia, intracranial hypertension, and cerebral intravascular sludging may all contribute to decreased neuronal viability during resuscitation. Global and regional brain injury require different therapeutic approaches. Treatment of global hypoxia should include adequate oxygenation, maintenance or increased CBF, control of cerebral edema, decrease in cerebral metabolic rates, and maintenance of systemic arterial blood pressure. This may involve controlled ventilation with increased inspired oxygen concentration, administration of dimethyl sulfoxide, phenytoin, low molecular weight dextran, and butyrolactone. On the other hand, following a regional hypoxic episode, therapy should be designed to decrease local cerebral vasoconstriction and thus shunt blood to ischemic areas (barbiturates), to maintain blood pressure (hemodilution or blood transfusion), to prevent platelet aggregation and intravascular sludging (aspirin or heparin), and to improve flow (revascularization techniques). Pharmacologic manipulation of neuro transmitter action offers considerable potential, as yet essentially unexplored. 115 References are cited.