Effect of gammahydroxybutyrate on intracranial pressure, mean systemic arterial pressure and cerebral perfusion pressure in experimentally induced brain oedema of the rat.

In the treatment of raised intracranial pressure (ICP) an agent is needed which can similarly reduce ICP and protect the brain without reducing systematic arterial pressure and cerebral perfusion pressure. Gammahydroxybutyrate (GHB) decreases cerebral metabolic requirement of oxygen (CMRO2) and glucose utilization rate. The effect of GHB on ICP, systemic arterial pressure and cerebral perfusion pressure in the experimentally induced brain oedema of the rat was examined. 400 mg/kg GHB reduced significantly ICP (11.74 +/- 1.20 mmHg; control: 16.20 +/- 8.89 mmHg; p less than 0.01) while increasing mean systemic arterial pressure (109.89 +/- 6.35 mmHg; control: 89.65 +/- 4.22 mmHg; p less than 0.05) and cerebral perfusion pressure (98.11 +/- 6.79 mmHg; control: 73.84 +/- 5.25 mmHg; p less than 0.02). In the dose-effect curve 200 mg/kg GHB show an increase in mean systemic arterial pressure from 89.60 +/- 9.35 mmHg to 98.60 +/- 3.48 mmHg (p less than 0.02) and 400 mg/kg GHB to 108.00 +/- 5.20 mmHg (p less than 0.001) mean systemic arterial pressure. The decrease in intracranial pressure is not due to a reduction in the mean systemic arterial pressure, but GHB does reduce the ICP while increasing mean systemic arterial pressure and cerebral perfusion pressure. GHB may be a useful adjunct to neurosurgical therapy in controlling elevated ICP.