OBJECTIVES: To assess the time course of biochemical responses to neonatal anoxia. METHODS: Neonatal anoxia was induced by placing 2-day-old rat pups into a glass chamber with 100% N(2) atmosphere, T=36.5 degrees C, for 20 minutes. The samples of serum, brain, lungs and liver were taken after 10 minutes, 2, 6, 12, 24 and 48 hours following the insult. The biochemical profile consisted of measurements of lactate, glutathione and the lysosomal enzyme N-acetyl-beta-D-glucosaminidase. RESULTS: Ten minutes after the insult, neonatal anoxia caused a threefold increase of the lactate level in serum as well as in all organs assessed, returning to control values in 2 hours. The profile of glutathione in the liver showed a time-dependent rise observed in both groups. No significant changes were seen in N-acetyl-beta-D-glucosaminidase response. CONCLUSIONS: The results indicate disruption of aerobic metabolism in our experimental model of neonatal anoxia, as proved by sharply increasing lactate levels. The rising glutathione level in the liver suggests improving antioxidant competences of the developing organism. Although the model used requires further specification, the obtained data are indicative of its usefulness in the study of neonatal anoxia.
OBJECTIVES: To assess the time course of biochemical responses to neonatal anoxia. METHODS:Neonatal anoxia was induced by placing 2-day-old rat pups into a glass chamber with 100% N(2) atmosphere, T=36.5 degrees C, for 20 minutes. The samples of serum, brain, lungs and liver were taken after 10 minutes, 2, 6, 12, 24 and 48 hours following the insult. The biochemical profile consisted of measurements of lactate, glutathione and the lysosomal enzyme N-acetyl-beta-D-glucosaminidase. RESULTS: Ten minutes after the insult, neonatal anoxia caused a threefold increase of the lactate level in serum as well as in all organs assessed, returning to control values in 2 hours. The profile of glutathione in the liver showed a time-dependent rise observed in both groups. No significant changes were seen in N-acetyl-beta-D-glucosaminidase response. CONCLUSIONS: The results indicate disruption of aerobic metabolism in our experimental model of neonatal anoxia, as proved by sharply increasing lactate levels. The rising glutathione level in the liver suggests improving antioxidant competences of the developing organism. Although the model used requires further specification, the obtained data are indicative of its usefulness in the study of neonatal anoxia.
Authors: Miroslav Pohanka; Hana Bandouchova; Jakub Sobotka; Jana Sedlackova; Ivana Soukupova; Jiri Pikula Journal: Sensors (Basel) Date: 2009-11-17 Impact factor: 3.576