Acute changes in regional cerebral metabolite values following experimental blunt head trauma

Abstract

A Remington humane stunner was used to deliver a blow to the left side of the surgically-exposed skull in ketamine-anesthetized cats. At 15 minutes after the trauma, brain tissue was frozen in situ. In animals without visible tissue hemorrhage (Grade 0) and in those with unilateral cerebral contusions involving the cerebral cortex and white matter (Grade 2), regional cerebral metabolite concentrations were measured by enzymatic-fluorometric techniques and edema was tested with an organic gradient. No substantial changes in cerebral metabolite concentrations were observed in head-injured animals without cerebral contusions. In animals with unilateral contusions, the white matter neighboring the tissue hemorrhage had an increase in lactic acid and a decrease in phosphocreatine as compared to values from corresponding areas on the contralateral side, and in control and Grade 0 animals. The cerebral cortex adjacent to tissue hemorrhage had a variable response that ranged from metabolite concentrations within normal ranges to marked decreases in high-energy phosphates and increases in lactic acid. Metabolites of the cortex and white matter contralateral as well as distant to contusion were not statistically different from values of control animals. Changes in several metabolites correlated well with the magnitude of edema. It is concluded that focal metabolic alterations can occur shortly after severe blunt head injury, and that these events may contribute to acute traumatic cerebral edema.

Early metabolic alterations in edematous perihematomal brain regions following experimental intracerebral hemorrhage

“…Indeed, we previously reported finding markedly higher lactate levels following blunt head trauma in edematous white matter located near brain contusions as compared with samples from noncontused hemispheres. 42 However, elevated tissue lactate levels are also observed 8 hours after severe fluid-percussion injury in the absence of hemorrhage 19 and after plasma infusions. 34 Also, our hematomal lactate levels are only 5 to 8 mol/g (data not shown), values that are considerably lower than those present in edematous white matter.…”

“…[40][41][42] Edema was quantitated by determining the water contents of white and gray matter samples from the brain regions listed earlier. Water content was determined by weighing and then drying the samples at 100˚C for at least 24 hours to a constant weight.…”

“…[40][41][42]46 The frozen heads were cut using a bandsaw into 5-mm-thick coronal sections. Subcortical white and cortical gray matter tissue specimens were sampled in a refrigerated glove box (Ϫ20˚C) at specific sites identified by their relationship to the hematoma.…”

Identifying traumatic brain injury in patients with isolated head trauma: are arterial lactate and base deficit as helpful as in polytrauma?

“…Wagner et al 24 showed a high increase in LAC concentration in the white matter within the territory of vasogenic oedema of contused area shortly after experimental head injury in an animal model. 24 Despite the availability of reasonable evidence on correlating cerebral LAC levels with severity of TBI, the diagnostic performance of arterial LAC and its ability to reflect CNS/CSF-LAC levels in patients with isolated head injury has been inadequately studied.…”

Changes in ICBF, morphology and related parameters by fluid percussion injury

“…This transient phenomenon may possibly contribute to the blood-brain barrier breakdown demonstrated by extravasation of Evans blue in the present study, and be associated with the immediate elevation of intracranial pressure and the development of oedema after fluid percussion brain injury in cats previously reported [19]. It also may play a role in mechanisms causing subsequent decrease in CBE…”