We describe a novel methodological approach for inducing cold lesion in the
mouse as a model of human cortical contusion trauma. To validate its repro
ducibility and reliability, dexamethasone (Dxm) was repeatedly applied to d
emonstrate possible antioedematous drug effects. Following tho induction of
anaesthesia with halothane, the dura was exposed via trephination. Using a
micromanipulator a pre-cooled (-78 degreesC) copper cylinder, 3 mm in diam
eter, was pressed down to a depth of 1 mm onto the dura fur 30 s under micr
oscopic control. The body temperature was held constant at 37 degreesC thro
ughout the procedure. Blood pressure (BP), measured by a modified photosens
or-monitored tail-cuff method, and acid-base status were not significantly
different when analysed before and after cold lesion and prior to sacrifice
. However, there was a marginal mixed respiratory and metabolic acidosis. T
he antioedematous action of Dxm was studied in four standard pre and post-t
reatment paradigms: 2x0.5 mg/kg (II), 2x12,5 mg/kg (III) and 4x6.25 mg/kg (
IV: 3x pre-, 1x post-treatment; V: 1x pre-, 3x post-treatment). Physiologic
al saline injections served as controls. High doses of Dxm (III-V) signific
antly attenuated the cold-lesion-induced loss of body mass. Dxm treatment a
lso resulted in a reduction of brain water content (III; P<0.05), and brain
swelling (IV; P<0.05) in the lesioned hemisphere, relative to controls. In
conclusion, we have characterized a novel cold lesion model in the mouse t
o mimic traumatic brain injury and the beneficial effect of Dxm treatment o
n the extent of brain oedema.