During the past decade, it has become increasingly clear that central nervous system trauma may produce tissue injury through both direct and indirect mechanisms.' Direct effects occur acutely as a result of mechanical disruption, with subsequent rapid cell death. Indirect effects are delayed and develop over a period of minutes to hours following the initial trauma. A variety of biochemical and physiological changes have been postulated to contribute to this delayed, secondary injury process, including: alterations in lipid metabolism: disruption of magnesium ion homeo~tasis,~ and edema formation! In the present study, preliminary results on changes in tissue lipids, magnesium, and edema following experimental traumatic brain injury to rats5 are reported. Any statistically significant differences among the control and experimental groups were determined by analysis of variance (ANOVA) with a Dunnett's posthoc test (* = significantly different from controls, p 5 0.05). Tissue levels of free fatty acids (FFA), total phospholipid, cholesterol, thromboxane B2, and water content were measured over time in the brains of rats subjected to fluid-percussion traumatic brain injury of moderate severity (2.0-2.2 atmospheres). 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 the area that has been shown histologically to be the site of maximal injury (left parietal cortex) was dissected out. Trauma resulted in small increases in FFA levels a t the site of injury a t 10 min and 4 h, and much larger increases a t 24 h. Among the FFA, the largest increases were observed in stearate (control = 1.5 k 0.1, 10 rnin = 6.9 k 0.1*, 4 h = 7.4 * Oh*, 24 h = 17 .3 f 1 . 1 * pg/mg protein) arachidonate (control = 0.1 f 0.01, 10 rnin = 0.6 + 0.02*, 4 hr = 1.2 + 0.1*, 24 hr = 2.4 f 0.2*) and docosahexaenoate (control = 0.1 * 0.01, 10 rnin = 0.1 + 0.01, 4 h = 1 . 1 f 0.1*, 24 h = 2.7 * 0.2*). Total brain phospholipid and cholesterol levels were significantly decreased at all postinjury time points studied. Thromboxane levels were markedly elevated a t 10 min postinjury, substantially declined by 4 h, and approached control values a t 24 h (control = 8.7 * 2.8, 10 rnin = 636.4 8.3 33.1, 4 h = 110.8 11.4, 24 hr = 18.1
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