Postnatal development of hepatocytes following oxygen deficiency in utero

Pregnant rats were exposed to altitude hypoxia (5,000 m = pO2 11.33 kPa) 8 h daily, from the 16th through 21st d of pregnancy. The livers of the newborn male rats were morphometrically examined by electron microscopy for both qualitative and quantitative parameters, on the 2nd, 5th, 11th and 22nd d of age and were compared with those of controls during the same periods of postnatal development. Substantive changes were exhibited by the mitochondria. Processes of autophagocytic decomposition were recorded (focal vacuolisation, formation of myelin structures). Volume densities on the 2nd (0.2041), 11th (0.2048), and 22nd (0.2495) d of age were clearly higher than in control animals and were all on a rising trend. Numerical density, on the other hand, trebled in the controls (0.0738 on the 2nd d and 0.2261 on the 22nd) and almost doubled in the hypoxia animals (0.0849 on the 2nd d and 0.1471 on the 22nd). In other words, the volume of the average mitochondrion was larger in hypoxia animals, whereas surface densities were lower. Hepatocytes differed from cardiomyocytes, in that increased autophagocytosis of mitochondria and glycogen was recordable from the former only on the 5th d. Glycogen levels of hepatocytes went up considerably, with the rise recorded from controls (0.0181 on the 2nd d and 0.1911 on the 22nd) being somewhat stronger than that observed from hypoxia animals (0.0276 on the 2nd d and 0.1742 on the 22nd). The changes postnatally recorded from liver cells in the wake of prenatal hypoxia are believed to be processes of adaptation which do not cause any irreversible damage.