Postinjury treatment with magnesium chloride attenuates cortical damage after traumatic brain injury in rats

The neuroprotective effect of magnesium chloride (MgCl2), a compound previo usly demonstrated to improve behavioral and neurochemical outcome in severa l models of experimental brain injury, was evaluated in the present study. Male Sprague-Dawley rats were anesthetized and subjected to lateral fluid-p ercussion brain injury of moderate severity (2.5-2.8 atm), A cannula was im planted in the left femoral vein and at 1 h following injury, animals rando mly received a 15 min i.v. infusion of either MgCl2 (125 mu mol/rat) or sal ine. A second group of animals received anesthesia, surgery, and either MgC l2 or vehicle to serve as uninjured (sham) controls, Two weeks following br ain injury, animals were sacrificed, brains removed, and coronal sections w ere taken for quantitative analysis of cortical lesion volume and hippocamp al CA(3) cell counts. Traumatic brain injury resulted in a lesion in the ip silateral cortex and loss of pyramidal neurons in the CA3 region of the hip pocampus in vehicle-treated animals (p < 0.01 vs. uninjured animals). Admin istration of MgCl2 significantly reduced the injury-induced damage in the c ortex (p < 0.01) but did not alter posttraumatic cell loss in the CA(3) reg ion of the ipsilateral hippocampus, The present study demonstrates that, in addition to its beneficial effects on behavioral outcome, MgCl2 treatment attenuates cortical histological damage when administered following traumat ic brain injury.