Prolonged postischemic hyperventilation reduces acute neuronal damage after 15 min of cardiac arrest in the dog.

Hyperventilation is commonly used as a constituent of antiedematous therapy after global cerebral ischemia. The effect of hyperventilation on brain functions, however, is complex, and a number of mechanisms involved remains unclear. In this study, we attempted to determine whether postischemic hyperventilation influences acute neuronal changes developing during recirculation. Two groups of dogs underwent 15 min of cardiac arrest and cardiopulmonary resuscitation with an 8 h survival. After resuscitation, in group A the internal environment was maintained in the physiological ranges. In group B the animals were artificially hyperventilated maintaining a high level of respiratory alkalosis during recirculation. Histopathological examination of the vulnerable structures was performed using the Nauta degenerating method and the argyrophilic neurons were counted. Statistically significant amelioration in group B suggests that postischemic hyperventilation may act as a neuroprotective factor.