Patients with severe traumatic brain injury resulting in increased intracranial pressure refractory to first-tier interventions challenge the critical care team. After exhausting these initial interventions, critical care practitioners may utilize barbiturate-induced coma in an attempt to reduce the intracranial pressure. Titrating appropriate levels of barbiturate is imperative. Underdosing the drug may fail to control the intracranial pressure, whereas overdosing may lead to untoward effects such as hypotension and cardiac compromise.
In rats, propranolol potentiated alcohol and pentobarbitone hypnosis, but not barbital sleeping time, indicating enzyme inhibition as a possible mechanism of potentiation. Propranolol showed anticonvulsant effect on normal and reserpine treated rats by MES test, but showed dose related lowering of MET. Probable mechanisms are discussed.
