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


METHODS
Randomized, placebo-controlled trial.


METHODS
Animal laboratory.


METHODS
Eighteen male Sprague-Dawley rats subjected to a focal cortical brain injury.


METHODS
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.


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.
Kroppenstedt
S N
SN
Department of Neurosurgery, Charité, Virchow Medical Center, Humboldt-University Berlin, Germany.
Stover
J F
JF
Unterberg
A W
AW
D000818:Animals; D001783:Blood Flow Velocity / Q000187:drug effects; D001784:Blood Gas Analysis; D001929:Brain Edema / Q000209:etiology*; D001930:Brain Injuries / Q000134:cerebrospinal fluid / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology*; D002316:Cardiotonic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D002555:Cerebrospinal Fluid / Q000737:chemistry* / Q000187:drug effects*; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D004195:Disease Models, Animal; D004298:Dopamine / Q000494:pharmacology / Q000627:therapeutic use*; D004353:Drug Evaluation, Preclinical; D018698:Glutamic Acid / Q000032:analysis* / Q000187:drug effects*; D019271:Hypoxanthine / Q000032:analysis*; D017078:Laser-Doppler Flowmetry; D008297:Male; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
D002316:Cardiotonic Agents; D019271:Hypoxanthine; D018698:Glutamic Acid; D004298:Dopamine