Magnesium protects against neurological deficit after brain injury.

摘要: The biochemical factors that mediate secondary or delayed damage to the central nervous system (CNS) remain speculative. We have recently demonstrated brain injury in rats causes a rapid decline intracellular free magnesium (Mg2+) and total concentrations is significantly correlated with severity of injury. In order further investigate relationship between Mg2+ injury, we examined effect treatment on posttraumatic neurological outcome following fluid-percussion (2.0 atm) rats. Since administration ATP-MgCl2 has been shown be beneficial variety models organ ischemia, also efficacy ATP alone experimental Animals treated low (12.5 μmol) high (125 dose MgCl2 at 30 min postinjury showed significant dose-dependent improvement function when compared saline-treated controls. Treatment caused no chronic outcome. MgCl2-treated animals change mean arterial blood pressure (MAP), whereas either transient but fall MAP (P<0.01) during drug-infusion period. Our results suggest effective limiting extent dysfunction traumatic rat.