Effects of magnesium sulfate on tissue lactate and malondialdehyde levels in experimental head trauma

Abstract

These results demonstrate that head trauma leads to an increase in brain tissue lactate and MDA levels, and MgSO4 suppresses the rise in contused tissue when given after head trauma.

The effect of magnesium sulphate infusion on the incidence and severity of emergence agitation in children undergoing adenotonsillectomy using sevoflurane anaesthesia

“…In addition, an apparent positive relationship between emergence agitation and the cortical lactate level was also observed , which the authors suggested could reflect greater neuronal activity . Intravenous magnesium sulphate suppresses the increase in brain lactate concentrations and improves the electroencephalographic changes in response to cerebral ischaemia and head trauma in experimental animals. In the clinical setting, the use of intra‐operative magnesium sulphate has been associated with reduced postoperative neurocognitive impairment .…”

Effects of halothane, isoflurane, and sevoflurane on lipid peroxidation following experimental closed head trauma in rats

“…Ozsüer et al (3) showed that MDA increases significantly in the injured hemisphere, starting from 30 min after the trauma and reaching a maximum level at 2 h, after which it gradually declines. Experimental and clinical studies also demonstrate early increases in MDA after head injury (24–26). We did not know of any previous experimental study testing the effect of inhalation agents on lipid peroxidation after brain injury; therefore, we gave inhalation agents for 15 min after brain injury.…”

EFFECTS OF COMBINED AND INDIVIDUAL USE OF NMDA RECEPTOR ANTAGONIST MAGNESIUM SULPHATE AND CASPASE-9 INHIBITOR z-LEDH-fmk IN EXPERIMENTAL SPINAL CORD INJURY

“…[29][30][31][32][33][34] MgSO 4 is an NMDA receptor antagonist, which has been used clinically as a neuroprotective agent for treating acute stroke and other conditions like preeclampsia, atrial fibrillation, myocardial infarction 29 and experimentally in animal models of brain injury. [35][36][37] Recent studies have demonstrated that necrosis is not the only mechanism in cell death; apoptosis also has a major role in this process. [38][39][40] Because apoptosis needs energy, heavily injured cells die via necrosis, but the surrounding mildly damaged neural tissue can lose cells via apoptosis.…”