Invited review: Physiological and pathophysiological responses to intermittent hypoxia.
- J A Neubauer
- Journal of applied physiology
The present study was carried out in order to determine pathogenetic mechanisms of the human minimal brain dysfunction syndrome caused by perinatal hypoxic states. In our animal model newborn rats were exposed to an hypobaric atmosphere for 10 hours daily during the first ten postnatal days, thus causing a moderate chronically intermittent hypoxia. After a three months life under normal conditions the now adult rats were sacrificed and the dentate area of the hippocampus was examined for posthypoxic ultrastructural changes. By means of a quantitative stereological method the cytoplasm of the neurons in the granular layer of the hippocampal formation was analyzed. The absolute number of ribosomes was found to be unchanged after 3 months recovery from early postnatal hypoxia. However, the rough endoplasmic reticulum in cells of postnatally hypoxia exposed animals showed lengthened membranes that were significantly less dense equipped with ribosomes. Most striking was an enhancement in the number of free polysomes. Thus, a permanent disturbance in the quality of the proteinsynthesis capability of these neurons was shown to be a long-lasting effect of postnatal hypoxia.