Dopamine

Kroppenstedt, S N; Stover, J F; Unterberg, A W (2000). Effects of dopamine on posttraumatic cerebral blood flow, brain edema, and cerebrospinal fluid glutamate and hypoxanthine concentrations. Critical Care Medicine, 28(12):3792-3798. Abstract OBJECTIVES: Dopamine is often used in the treatment of traumatic brain injury to maintain cerebral perfusion pressure. However, it remains unclear whether dopamine contributes to secondary brain injury caused by vasoconstriction and resulting diminished cerebral perfusion. The present study investigated the effects of dopamine in different concentrations on posttraumatic cortical 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 brain injury. INTERVENTIONS: Four hours after controlled cortical impact, rats were randomized to receive physiologic saline solution (n = 6), 10-12 tig/kg/min dopamine (n = 6), or 40-50 microg/kg/min dopamine (n = 6), for 3 hrs. Cortical CBF was measured over both hemispheres by using laser-Doppler flowmetry before trauma and before, during, and after the infusion period. At 8 hrs after trauma, brains were removed to determine hemispheric swelling and water content. Cisternal cerebrospinal fluid was sampled to measure glutamate and hypoxanthine. 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 ig/kg/min dopamine did not change mean arterial blood pressure (MABP) or cortical CBF. However, infusion of 40-50 microg/kg/min dopamine, which elevated MABP from 89 to 120 mm Hg, significantly increased posttraumatic CBF within and around the contusion by 35%. Over the nontraumatized hemisphere, CBF remained unchanged. Hemispheric swelling, water content, cerebrospinal fluid glutamate, and hypoxanthine levels were not affected by dopamine in the given dosages. CONCLUSIONS: Under the present study design, there was no evidence for a dopamine-mediated vasoconstriction, because posttraumatic cortical CBF was increased by dopamine-induced elevation of MABP. However, the increase in CBF did not significantly affect edema formation or cerebrospinal fluid glutamate and hypoxanthine levels.

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Effects of dopamine on posttraumatic cerebral blood flow, brain edema, and cerebrospinal fluid glutamate and hypoxanthine concentrations. Critical Care Medicine, 28(12):3792-3798.

Transcript of Dopamine

Kroppenstedt, S N; Stover, J F; Unterberg, A W (2000). Effects of dopamine onposttraumatic cerebral blood flow, brain edema, and cerebrospinal fluid

glutamate and hypoxanthine concentrations. Critical Care Medicine,28(12):3792-3798.

Abstract

OBJECTIVES: Dopamine is often used in the treatment of traumatic brain injury tomaintain cerebral perfusion pressure. However, it remains unclear whether dopaminecontributes to secondary brain injury caused by vasoconstriction and resultingdiminished cerebral perfusion. The present study investigated the effects of dopaminein different concentrations on posttraumatic cortical cerebral blood flow (CBF), brainedema formation, and cerebrospinal fluid concentrations of glutamate andhypoxanthine. DESIGN: Randomized, placebo-controlled trial. SETTING: Animallaboratory. SUBJECTS: Eighteen male Sprague-Dawley rats subjected to a focal corticalbrain injury. INTERVENTIONS: Four hours after controlled cortical impact, rats wererandomized to receive physiologic saline solution (n = 6), 10-12 tig/kg/min dopamine(n = 6), or 40-50 microg/kg/min dopamine (n = 6), for 3 hrs. Cortical CBF wasmeasured over both hemispheres by using laser-Doppler flowmetry before trauma andbefore, during, and after the infusion period. At 8 hrs after trauma, brains wereremoved to determine hemispheric swelling and water content. Cisternal cerebrospinalfluid was sampled to measure glutamate and hypoxanthine. MEASUREMENTS ANDMAIN RESULTS: After trauma, cortical CBF was significantly decreased by 46% withinthe vicinity of the cortical contusion in all rats. Infusion of saline and 10-12 ig/kg/mindopamine did not change mean arterial blood pressure (MABP) or cortical CBF.However, infusion of 40-50 microg/kg/min dopamine, which elevated MABP from 89 to120 mm Hg, significantly increased posttraumatic CBF within and around the contusionby 35%. Over the nontraumatized hemisphere, CBF remained unchanged. Hemisphericswelling, water content, cerebrospinal fluid glutamate, and hypoxanthine levels werenot affected by dopamine in the given dosages. CONCLUSIONS: Under the presentstudy design, there was no evidence for a dopamine-mediated vasoconstriction,because posttraumatic cortical CBF was increased by dopamine-induced elevation ofMABP. However, the increase in CBF did not significantly affect edema formation orcerebrospinal fluid glutamate and hypoxanthine levels.