Objectives: The tissue damage due to hypoxia in newborns is to some extent age-dependent; organs of premature babies are more vulnerable to hypoxic insult than full-term neonates. The aim of this immunohistochemical study was to investigate the role of heat shock protein 70 (HSP70), a stress-inducible protein, in developing the response to hypoxia in premature newborns.
Methods: Postnatal day-7 rats (corresponding to a human fetus of 32-34 weeks' gestation) and day-12 rats (corresponding to a full-term newborn infant) (n = 7) were subjected to mild hypoxia at 33 degrees C. Control rats (n = 7) for each group breathed room air for 4 h. After 4 h of recovery, the animals were killed, and brains, hearts and kidneys were removed for immunohistochemical staining.
Results: Immunohistochemically, HSP70 expression was found to be induced in the hippocampus and myocardium after exposure to hypoxia. The level of HSP70 expression in the hippocampus after hypoxic stress was significantly higher in the 12-day rats than in the 7-day rats (p = 0.03). However, HSP70 expression in the myocardium did not show any significant difference between the two groups. In addition, no significant induction of HSP70 expression was apparent in the kidney of rats exposed to hypoxia or in any organ of the control animals.
Conclusions: We conclude that diminished HSP70 expression in the hippocampus of premature newborns may play a critical role in developing the response to hypoxic stress. However, HSP70 expression in the heart and the kidney after exposure to hypoxia did not appear to be related to fetal maturity.
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