Experimental brain injury in the dog

Abstract

✓ Brain injury was created in anesthetized dogs by the inflation and subsequent deflation of an epidural balloon. Animals in which intracranial pressure (ICP) increased to 40 torr within 3 hours after balloon removal were included in a randomized treatment protocol that included three treatment groups. Group I (control animals) received no additional treatment. Group II animals received 40 mg/kg pentobarbital initially, plus hourly doses. Group III animals received sufficient sodium nitroprusside to reduce systemic arterial pressure (SAP) to 80 to 90 torr. Pentobarbital reduced ICP compared to control animals, but cerebral perfusion pressure (CPP) was also reduced. Barbiturate treatment also prevented plateau waves. Progressive parallel deterioration in CPP occurred with time in control and pentobarbital-treated animals. The viability of the central nervous system was not improved by pentobarbital. Profound systemic hypotension, a major complication of pentobarbital treatment, required mephentermine to reverse it. Sodium nitroprusside failed to reduce ICP and caused a rapid, profound deterioration in CPP which far exceeded that observed in control or barbiturate-treated animals. Plateau waves were not prevented by nitroprusside. Barbiturates were more potent than nitroprusside in combatting systemic hypertension caused by elevated ICP. Pentobarbital may act by suppression of a central neurogenic mechanism for systemic hypertension and cerebral vasoparalysis. As a cerebral vasodilator, nitroprusside when used in the presence of an intracranial mass, brain edema, or cerebral vasoparalysis, will cause a rise in ICP and a fall in SAP, as well as a drastic reduction in CPP. Its use is probably contraindicated in these situations. Furthermore, it is inferior to barbiturates in reducing ICP and SAP and in preventing plateau waves.