Postnatal development of myocardial cells after oxygen deficiency in utero

Pregnant rats were kept at a simulated altitude hypoxia (5000 m = pO2 11.38 kPa) for eight hours every day from the 16th to 21st day of pregnancy. The heart musculature of the left ventricle of newborn male rats underwent electron microscopic qualitative and morphometric quantitative examinations on the 2nd, 5th, 11th and 22nd day. Prenatal hypoxia leads to delayed development of the heart. The reduced weight on the 2nd day compared with that of control animals is compensated on the 22nd day. Prenatal hypoxia causes matrix disintegration and cristolysis of the mitochondria. Volume density, which is lower on the 2nd day (0.24: 0.29 (control animals], reaches that of the controls by the 22nd day. But the specific surface density of the cristae mitochondriales is markedly higher in the animals subjected to hypoxia (2nd day 31.0: 20.6; 22nd day 44.0: 38.1). Prenatal hypoxia causes an increase, in the postnatal period, in the autophagocytosis processes, which normally already exist in the heart musculature; this is recognizable by an increase in the volume density of the autophagic vacuoles (2nd day 0.0049: 0.0034; 22nd day 0.0098: 0.0045). The changes observed are regarded as reversible, i.e. as adaptive processes.