effect of mild hypothermia on jugular venous bulb oxygen saturation and CSF glutamate in severe head trauma

Hypothermia has been used as a method of brain protection in patients with traumatic brain injury for many years. The protective effects of hypothermia are related to the inhibition of the excitatory amino acids [EAA] release including glutamate. The hypothermic decline of the cerebral metabolic rate of oxygen [CMRO[2]] is also another mechanism of brain protection because it maintains the aerobic metabolism of the brain. To study the effect of mild hypothermia on brain oxygenation and the release of the EAA glutamate in severe head trauma. Forty two patients [16 - 60 years old] with severe head trauma [Glasgow coma scale < 8] were classified according to the diagnosis by computed tomography into group 1 [global brain damage] [n=20] and group 2 [focal brain damage] [n=22] two cases in group 2 were died before completion of the study so they were excluded. The cerebrospinal [CSF] glutamate, the jugular venous bulb oxygen saturation, the jugular venous lactate, the Glasgow coma scale [GCS], the acute physiological and chronic health evaluation score [APACHE II] and the length of lCU stay and other hemodynamic variables were measured and recorded. Hypothermia decreased the cerebrospinal [CSF] glutamate, improved the jugular venous bulb oxygen saturation, decreased the jugular venous lactate, improved the Glasgow coma scale [GCS] and decreased the acute physiological and chronic health evaluation score [APACHE II], There were significant statistical differences [p < 0.001] in each group but there were no statistical significant differences between both groups. The length of ICU stay was shorter in the group 1 than in group 2. Mild Hypothermia is one of the mechanisms of brain protections through decreasing the level of the neurotoxic cerebrospinal excitatory amino acid glutamate and by improving the cerebral oxygenation and preventing the anaerobic metabolism by decreasing the level of serum lactate

Effects of MK-801 (dizocilpine) on Brain Cell Membrane Function and Energy Metabolism in Experimental Escherichia coli Meningitis in the Newborn Piglet

We evaluated the efficacy of non-competitive N-methyl-D-aspartate receptor antagonist MK-801 (dizocilpine) as an adjuvant therapy in experimental neonal bacterial meningitis. Meningitis was induced by injecting 10(6) colony forming units of Escherichia coli into the cisterna magna. MK-801 3 mg/kg was given as a bolus intravenous injection, 30 min before the induction of meningitis. MK-801 did not down-modulate the inflammatory parameters, such as increased intracranial pressure, cerebrospinal fluid (CSF) leukocytosis, increased lactate and TNF-alpha levels in the CSF, and hypoglycorrhachia observed in the meningitis group. MK-801 did not significantly attenuate the elevated glutamate concentration in the CSF. However, MK-801 showed some neuroprotective effects as evidenced by significant attenuation of cerebral lipid peroxidation products (conjugated dienes) and increase of brain high-energy phosphate compounds (ATP and PCr). Improvement in cerebral cortical cell membrane Na+, K+ -ATPase activity did not reach a statistical significance. These results suggest that MK-801 was effective in ameliorating brain injury in neonatal bacterial meningitis, although it failed to attenuate the inflammatory responses.