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Journal of neurotrauma · Jan 1988
Traumatic brain injury in the rat: effects on lipid metabolism, tissue magnesium, and water content.
- P Demediuk, A I Faden, R Romhanyi, R Vink, and T K McIntosh.
- Department of Neurology, University of California, San Francisco.
- J. Neurotrauma. 1988 Jan 1; 5 (2): 105-19.
AbstractTissue levels of free fatty acids (FFA), total phospholipid, cholesterol, thromboxane B2, water, Na+, K+, and Mg2+ were measured in rat brain after lateral fluid-percussion brain injury of moderate severity (2.0-2.2 atm). Brains of injured animals and sham-operated controls were frozen in situ with liquid N2 at 10 min, 4 h, and 24 h postinjury and removed. The left parietal cortex, which has been shown previously histologically to be the site of maximal injury, was dissected for analysis. Traumatic injury was associated with small increases in FFA levels at 10 min and 4 h and much larger increases at 24 h postinjury. Among the FFA, the largest increases were observed in stearate, arachidonate, and docosahexaenoate. Total phospholipid and cholesterol levels were decreased significantly at all experimental time points. Thromboxane levels were markedly elevated (30-fold) at 10 min posttrauma but substantially declined by 4 h and approached control values at 24 h. Total Mg2+ levels were significantly below control values at 4 h and 24 h posttrauma. No changes in water content were observed at any of these time points. Small decreases in tissue K+ occurred at 4 h; tissue Na+ levels were found to be slightly increased only at 24 h. These results are consistent with the hypothesis that changes in lipid metabolism and Mg2+ content of brain after injury may play a role in the pathophysiology of irreversible, posttraumatic tissue damage. In contrast, significant edema formation does not occur in this model and does not, therefore, appear to be a factor in the injury process.
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