The frequency-domain multiple-distance (FDMD) method is capable of measuring the absolute absorption and reduced scattering coefficients of optically turbid media. Absolute measurement of absorption at two near-infrared (NIR) wavelengths makes possible the quantitation of tissue haemoglobin concentration and tissue haemoglobin oxygen-saturation (StO2). However, errors are introduced by the uncertainties of background absorption and the dissimilarities between real tissues and the simplified mathematical model on which these measurements are based. An FDMD-based tissue instrument has been used for the monitoring of tissue haemoglobin concentration and oxygenation in the brain of newborn piglets during periods of hypoxia and hyperoxia. These tissue haemoglobin saturation values were compared with arterial saturation (SaO2) and venous saturation (SvO2) measured by blood gas analyses. A linear correlation was observed between StO2 and the average of SaO2 and SvO2. However, StO2 is not equal to any fixed weighted average of SaO2 and SvO2 unless we introduce an effective background tissue absorption. The magnitude of the background absorption was about 0.08 cm(-1) at 758 nm and 0.06 cm(-1) at 830 nm, and it was nearly consistent between piglets. The origin of this 'effective' background absorption may be real, an artefact caused by the application of a simplified model to a complex sample, or a combination of factors.

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Magnesium is a non-competitive antagonist of the NMDA receptor. Hypoxic insults to the brain are associated with a significant increase in the intranuclear Ca(2+) due to altered nuclear membrane Ca(2+) influx mechanisms including hypoxia-induced modifications of nuclear membrane IP(3) receptors. In this study we have examined the effects of magnesium sulfate administration to newborn piglets subjected to normoxia and severe hypoxia. The animals were randomly divided into normoxic (n=4), hypoxic (n=4) and magnesium sulfate treated hypoxic (n=4) groups. Hypoxia was confirmed biochemically by measuring ATP and phosphocreatine (PCr) levels in the brain tissue. Intranuclear Ca(2+) influx was assessed by measuring (45)Ca(2+) uptake. Results show a significant (P<0.05) decrease in ATP and PCr levels in hypoxic group in comparison with normoxia. On the other hand magnesium-treated hypoxic group showed a significantly (P<0.05) higher ATP and PCr in comparison with the hypoxic group. Intranuclear Ca(2+) was significantly (P<0.05) higher in the hypoxic group in comparison with both normoxic and magnesium-treated hypoxic groups. In addition results show that magnesium prevented hypoxia-induced modification of the IP(3) receptor. Magnesium treatment significantly reduced the hypoxia-induced increase in the number of receptors (reduced B(max) --P<0.05-treated hypoxia vs. hypoxia and normoxia), and reversed the receptor affinity (reduced dissociation coefficient-K(d)--P<0.05-treated hypoxia vs. normoxia). The results demonstrate that the administration of magnesium sulfate prior to hypoxia prevents the hypoxia-induced increase in intranuclear Ca(2+) and IP(3) receptor modifications. We conclude that Mg(2+ )administration prevents hypoxia-induced modification of neuronal nuclear membrane function that leads to intranuclear Ca(2+)-dependent transcription of apoptotic proteins leading to hypoxic neuronal programmed cell death.

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To test the hypothesis that acute hypoglycemia leads to free radical induced alterations in cerebral mitochondria, newborn piglets were subjected to 2 h of insulin-induced hypoglycemia (blood glucose 1 mmol/l). The effects of free radicals were determined in cerebral cortical synaptosomes, mitochondria, and neuronal nuclei by measuring membrane lipid peroxidation. Fragmentation of nuclear and mitochondrial DNA was also examined. Lipid peroxidation was significantly increased in hypoglycemic mitochondrial membranes as compared to controls, but no increase in peroxidation in hypoglycemic synaptosomal or nuclear membranes was observed. An increase in low molecular weight DNA fragments was observed only in mitochondrial DNA from hypoglycemic piglets. We speculate that alteration of cerebral mitochondria due to increased free radical production is one of the early events in the pathogenesis of hypoglycemic brain injury.