Effects of dopamine on posttraumatic cerebral blood flow, brain edema, andcerebrospinal fluid glutamate and hypoxanthine concentrations

Objectives: Dopamine is often used in the treatment of traumatic brain inju ry to maintain cerebral perfusion pressure. However, it remains unclear whe ther dopamine contributes to secondary brain injury caused by vasoconstrict ion and resulting diminished cerebral perfusion. The present study investig ated the effects of dopamine in different concentrations on posttraumatic c ortical cerebral blood flow (CBF), brain edema formation, and cerebrospinal fluid concentrations of glutamate and hypoxanthine. Design: Randomized, placebo-controlled trial. Setting: Animal laboratory. Subjects: Eighteen male Sprague-Dawley rats subjected to a focal cortical b rain injury. Interventions: Four hours after controlled cortical impact, rats were rando mized to receive physiologic saline solution (n = 6), 10-42 mug/kg/min dopa mine (n = 6), or 40-50 mug/kg/min dopamine (n = 6), for 3 hrs. Cortical GBF was measured over both hemispheres by using laser-Doppler flowmetry before trauma and before, during, and after the infusion period. At 8 hrs after t rauma, brains were removed to determine hemispheric swelling and water cont ent. Cisternal cerebrospinal fluid was sampled to measure glutamate and hyp oxanthine. Measurements and Main Results: After trauma, cortical CBF was significantly decreased by 46% within the vicinity of the cortical contusion in all rats . Infusion of saline and 10-12 mug/kg/min dopamine did not change mean arte rial blood pressure (MABP) or cortical CBF. However, infusion of 40-50 mug/ kg/min dopamine, which elevated MABP from 89 to 120 mm Hg, significantly in creased posttraumatic CBF within and around the contusion by 35%. Over the nontraumatized hemisphere, CBF remained unchanged. Hemispheric swelling, wa ter content, cerebrospinal fluid glutamate, and hypoxanthine levels were no t affected by dopamine in the given dosages. Conclusions: Under the present study design, there was no evidence for a do pamine-mediated vasoconstriction, because posttraumatic cortical GBF was in creased by dopamine-induced elevation of MABP, However, the increase in CBF did not significantly affect edema formation or cerebrospinal fluid glutam ate and hypoxanthine levels.