pH-associated Brain Injury in Cerebral Ischemia and Circulatory Arrest

Abstract

Neuronal injury remains a major limitation in therapies directed toward cardiopulmonary resuscitation and cerebral ischemia. We summarize clinical and experimental information regarding pH-modulated mechanisms of cerebral ischemic injury and the status of antiacidosis therapies relative to the brain. A large body of evidence in animals and humans indicates that cerebral pH can modulate, and perhaps mediate, ischemic brain pathology and influence functional outcome. The importance of low pH and brain bicarbonate levels during reperfusion as a secondary injury remains an open question of therapeutic importance. Under specific conditions, acidosis may be neuroprotective, but this is an area of current controversy. Effective antiacidosis therapy must address the possibility of synergism and competition among multiple injury mechanisms.