Effects of magnesium administration on brain edema and blood-brain barrier breakdown after experimental traumatic brain injury in rats.
In this study, we examined the effects of magnesium sulfate administration on brain edema and blood-brain barrier breakdown after experimental traumatic brain injury in rats. Seventy-one adult male Sprague-Dawley rats were anesthetized, and experimental closed head trauma was induced by allowing a 450-g weight to fall from a 2-m height onto a metallic disk fixed to the intact skull. Sixty-eight surviving rats were randomly assigned to receive an intraperitoneal bolus of either 750 micromol/kg magnesium sulfate (group 4; n = 30) or 1 mL of saline (group 2; n = 30) 30 minutes after induction of traumatic brain injury; 39 nontraumatized animals received saline (group 1; n = 21) or magnesium sulfate (group 3; n = 18) with an identical protocol of administration. Brain water content and brain tissue specific gravity, as indicators of brain edema, were measured 24 hours after traumatic brain injury. Blood-brain barrier integrity was evaluated quantitatively 24 hours after injury by spectrophotometric assay of Evans blue dye extravasations. In the magnesium-treated injured group, brain water content was significantly reduced (left hemisphere: group 2, 83.2 +/- 0.8; group 4, 78.4 +/- 0.7 [P <.05]; right hemisphere: group 2, 83.1 +/- 0.7; group 4, 78.4 +/- 0.5. [P <.05]) and brain tissue specific gravity was significantly increased (left hemisphere: group 2, 1.0391 +/- 0.0008; group 4, 1.0437 +/- 0.001 [P <.05]; right hemisphere, group 2, 1.0384 +/- 0.001; group 4, 1.0442 +/- 0.005 [P <.05]) compared with the saline-treated injured group. Evans blue dye content in the brain tissue was significantly decreased in the magnesium-treated injured group (left hemisphere: group 2, 0.0204 +/- 0.03; group 4, 0.0013 +/- 0.0002 [P <.05]; right hemisphere: group 2, 0.0064 +/- 0.0009; group 4, 0.0013 +/- 0.0003 [P <.05]) compared with the saline-treated injured group. The findings of the present study support that beneficial effects of magnesium sulfate exist after severe traumatic brain injury in rats. These results also indicate that a blood-brain barrier permeability defect occurs after this model of diffuse traumatic brain injury, and magnesium seems to attenuate this defect.
Esen
Figen
F
Department of Anesthesiology and Intensive Care, University of Istanbul, Istanbul Faculty of Medicine, Istanbul, Turkey. esenf@istanbul.edu.tr
Erdem
Tulin
T
Aktan
Damla
D
Kalayci
Rivaze
R
Cakar
Nahit
N
Kaya
Mehmet
M
Telci
Lutfi
L
D000818:Animals; D001784:Blood Gas Analysis; D001812:Blood-Brain Barrier / Q000187:drug effects*; D001831:Body Temperature / Q000187:drug effects; D001834:Body Water / Q000378:metabolism / Q000502:physiology; D001929:Brain Edema / Q000473:pathology*; D001930:Brain Injuries / Q000473:pathology*; D004396:Coloring Agents; D005070:Evans Blue; D007839:Functional Laterality / Q000502:physiology; D006439:Hemodynamics / Q000187:drug effects; D008274:Magnesium / Q000494:pharmacology*; D008297:Male; D010539:Permeability / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013046:Specific Gravity
D004396:Coloring Agents; D005070:Evans Blue; D008274:Magnesium