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Journal Article 2006; 27(Suppl 2): 78-81 PubMed PMID: 17159785 Citation  Keywords:  Acetylglucosaminidase:analysis, Animals, Animals, Newborn, Biomarkers:analysis, Brain Chemistry, Disease Models, Animal, Female, Glutathione:analysis, Hypoxia:metabolism, Lactic Acid:analysis, Liver:chemistry, Lung:chemistry, Rats, Rats, Wistar,.   

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....

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Journal Article 2004; 25(5): 361-367 PubMed PMID: 15580171 Citation  Keywords:  Altitude, Animals, Body Weight:physiology, Cysteamine:pharmacology, Growth Hormone:genetics, Hypothalamus:drug effects, Hypoxia:metabolism, Male, Pituitary Gland:metabolism, RNA, Messenger:analysis, Rats, Rats, Sprague-Dawley, Somatostatin:drug effects,.   

OBJECTIVES: The aim of this study was to investigate the response of the growth hormone (GH) in rat anterior pituitary to intermittent hypoxia (IH) and its modulation by hypothalamic somatostatin (SS).

SETTING AND DESIGN: To observe the hypoxic response, rats were exposed to simulated altitude hypoxia (2 km or 5 km) in a hypobaric chamber for various days (4 h/d); to clarify SS-involvement, rats were pretreated with SS antagonist (cysteamine, CSH, 200 mg/kg/d, s.c.) then exposed to IH (5 km) for 2d. The GH mRNA and immunostaining GH in pituitary as well as immunostaining SS in median eminence (ME) of hypothalamus were assayed by RT-PCR and immuno-histochemistry, respectively.

RESULTS: IH of 5 km altitude (IH5) markedly suppressed the body weight gain (BWG) of rats from 1d to 10d, and it was returned to control level henceforth, while no significant influence was showed in the group of IH of 2 km altitude (IH2). IH5 for 2 and 5d significantly decreased GH mRNA expression in the pituitary. The pituitary immunostaining GH was remarkably increased in groups of IH2 for 5, 10, and 15 d, and in groups of IH5 for 2, 5, and 10d. Immunostaining SS in ME was significantly reduced in group of IH2 for 5d, and in groups of IH5 for 2d and 5d. Pretreatments (s.c.) with SS antagonist (CSH) significantly reversed IH5-caused increase of immunostaining GH and reduction of mRNA levels in pituitary.

CONCLUSIONS: IH may cause a short-term and recoverable suppression of GH release, and reduce GH mRNA expression in anterior pituitary, which may depend on the intensity and duration of the hypoxia. This suppression may be due to a modulation of hypoxia-activated SS....

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