Effect of THAM on Brain Oedema in Experimental Brain Injury

Summary

The metabolic brain acidosis after trauma has been thought to increase brain oedema and contribute to neurologic deterioration. Amelioration of the brain acidosis either by systemic buffering agents or by hyperventilation has been proposed as a method of treatment. The objective of this study was to explore brain oedema and the metabolic changes in brain that occur with the use of hyperventilation, Tromethamine and combination (THAM and hyperventilation) therapy in experimental fluid-percussion brain injury. Brain lactate, brain pH, inorganic phosphate (Pi) and ATP were measured by ¹H and ³¹P magnetic resonance spectroscopy. Also Water content in brain tissue using the specific gravimetric technique were determined in 32 cats. Prolonged hyperventilation provided relative ischaemia in brain tissue and promoted more production of brain lactate, no recovery of PCr/Pi ratio, and no decrease in brain oedema. On the other hand the administration of THAM served to decrease production of brain lactate and brain oedema and promoted the recovery of cerebral energy dysfunction. THAM ameliorates the deleterious effects of hyperventilation by minimizing energy disturbance and also decreases brain oedema. We conclude that THAM may be effective in reducing brain tissue acidosis and helpful as a metabolic stabilizing agent following severe head injury.

This work was supported in part by grants NS 12587 and NS 19235 from the National Institute of Health. Additional facilities and support were provided by the Richard Roland Reynolds Neurosurgical Research Laboratories.