No abstract

Previous studies have shown contradictory results regarding magnesium-mediated neuroprotection in animal models of perinatal asphyxia. The aim of this study is to investigate the effects of MgSO(4) postasphyxial treatment on hypoxia-ischemia (HI)-induced brain injury in neonatal rats and the possibility that this effect is related to the severity of brain damage. Seven-day-old rats underwent unilateral carotid artery ligation followed by 1 or 2 hours of hypoxia (8% O(2)) and MgSO(4) administration. Adenosine triphosphate/phosphocreatine and glutamate/glutamine measurements and neuropathological evaluation of the hippocampus were used to assess the effects of HI and MgSO(4). HI caused time-dependent changes in energy stores, amino acid concentrations, and brain damage. Administration of MgSO(4) after 1 hour but not after 2 hours of hypoxia resulted in significant prevention of HI-induced brain injury. MgSO(4) administration results in a significant protection against moderate HI-induced brain damage, whereas it fails to offer a similar effect against severe brain damage.

Perinatal asphyxia (PA) is a major determinant for long-term sensorimotor and locomotor deficits. The model of neonatal hypoxia-ischemia (HI) in 7-day-old rats produces sensorimotor cortex, thalamus and striatum injury, which are all critical for the maintenance of sensory motor function. The aim of this study was to evaluate the long-term neurodevelopmental disturbances in the above experimental model and to assess the neuroprotective effect of MgSO₄ in terms of long-term behavioral and morphological changes. Seven-day-old rats were separated into three groups: A (control), neither ligated nor exposed to hypoxia; B (HI/MgSO₄) ligated, exposed to hypoxia and treated with MgSO₄ (2 g/kg b.w., i.p.), and C (HI) ligated and exposed to hypoxia. At the age of 42 days, the behavior of the rats was evaluated using 5 sensorimotor tests. Muscle power, motor coordination, reflexes, and limb placing were tested to different sensory stimuli. The study was completed with the histopathological evaluation of brain tissue damage. In all individual tests the HI-treated rats performed significantly worse than the control and MgSO₄-treated rats and this difference was more pronounced in the limb placing tests. Additionally, neonatal HI resulted in extensive neuronal damage that was limited after MgSO₄ administration. Behavioral alterations represent a useful endpoint for studying the consequences of a perinatal HI insult and the efficacy of potential neuroprotective treatments. MgSO₄ administration resulted in prevention of HI-induced sensorimotor deficits and brain injury.

Our results indicate that it is possible, when using the BLES device, to completely excise small (≤ 10 mm) breast carcinomas that appear radiologically as solid lesions. This subset of patients should be investigated regarding the therapeutic potential of this method.