Abstract
Much of the tissue damage resulting from trauma to the central nervous system appears to result from secondary, delayed biochemical changes that follow primary mechanical injury. However, the early biochemical events remain to be elucidated. In the present studies, we have used phosphorus (31P) magnetic resonance spectroscopy (MRS) to examine in vivo, the temporal changes in brain intracellular free Mg2+ concentration following fluid percussion head injury in rats. We report that injury caused a profound and rapid decrease in intracellular free Mg2+ which was significantly correlated with the severity of injury. At high levels of injury, the decrease in intracellular free Mg2+ concentration was associated with a decrease in total Mg2+ concentration as determined by atomic absorption spectrophotometry. Prophylactic treatment with MgSO4 prevented the post-traumatic decrease in intracellular free Mg2+ and resulted in a significant improvement in acute neurological outcome. Because magnesium is essential for a number of critical enzyme reactions, including those of glycolysis, oxidative and substrate level phosphorylation, protein synthesis, and phospholipid synthesis, changes in free Mg2+ after brain trauma may represent a critical early factor leading to irreversible tissue damage.
Highlights
The correlationbetween post-traumatic freeMg2+depletion The chemical shift of ATP may be affected by factors and neurological outcome raised the possibility that theM$C other than M2+, such as pH, temperature, and the binding changemightbe causally relatedtothe secondary tissue of other cations (15, 16)
Intracellular pH changes have injury, there was no post-traumatic decline in free Mg2+in been observed in this model of brain injury (6); we
MgS04-treated animals in contrast to saline-treated controlshave shown that these changes are small and transient, with who showed approximately a 79% decrease in free Mg" intracellular pH returning to pre-injuryvalues by 60-90 min concentration by 3 h (Table 111).the prophylac- post-trauma (8, 9, 24; Fig. 2)
Summary
Effect of prophylactic MgSO, infusion upon intracellular Mfgr"ee concentration and upon acute neurological outcome, following traumatic brain injury inthe rat Animals ( n = 5) were given either 15 meq/literblood MgS04 intravenously or saline (equal volume) 5 minimmediatelyprior to severe (2.0 & 0.5) fluid percussion brain injury. Free MgZ' concentrations are reported as mean -C S.D. Animals subjected to low injury showed minimal neurologcoMmpeaonsite ical deficits at 24 h (mean compositescore = 12); animals that received high injury had a marked deficit at 24 h (mean compositescore = 7)(Table 11).
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