The effects of local intraparenchymal pentobarbital on intracranial hypertension following experimental subarachnoid hemorrhage.

Barbiturates are often utilized clinically in circumstances in which elevated intracranial pressure is expected. In this study, the mechanism of action of barbiturates was examined in dogs with intracranial hypertension induced by injecting autogenous incubated blood into the chiasmatic cistern. Intracranial pressure and systemic blood pressure were continuously monitored. A single bilateral administration of powdered pentobarbital (2 mg and 0.4 mg) in experimental animals and solid d-glucose (2 mg) in control animals was given into the posterior hypothalamus, pontine reticular formation, or medullary reticular formation when intracranial pressure reached 20-30 mmHg after the blood injection--usually in 3-6 h. The increased intracranial pressure following the experimental subarachnoid hemorrhage was always associated with either intracranial pressure irregularities or concomitant blood pressure variations, suggesting the presence of vasomotor instability. Administration of both 2 mg and 0.4 mg of pentobarbital into the medulla caused a significant (P less than 0.01) decrease of the intracranial pressure to 44 and 65% of control and stabilization of the intracranial pressure irregularities, whereas pentobarbital given at the other sites did not. The blood pressure was also decreased significantly (P less than 0.01) to 80 and 88% of control and the blood pressure variations were stabilized in animals after administration of pentobarbital into the medulla, whereas in those given pentobarbital at the other sites, it was not. The results suggest that, in the presence of elevated intracranial pressure following experimental subarachnoid hemorrhage, the mechanisms of action of barbiturates in reducing the intracranial pressure may result from alleviation of cerebral vasomotor instability by depression of the vasomotor center of the medulla.