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The brain lesions produced by temporary arrest of circulation in a newborn and an 11-month-old infant are described. In the newborn, two periods of arrest occurred, one on the fifth day after birth and the second a few day before death on the sixth week. The older infant suffered a single episode of cardiac arrest at the age of 11 months and survived 8 days. In both cases, postmortem examination revealed lesions in spinal cord, in brain stem, and in cerebral hemispheres. This distribution of damage is compared with the patterns of injury produced experimentally by episodes of partial (hypoxia) and total (anoxia) asphyxia in subhuman primates. The coexistence of hemispheral and brain stem nuclear patterns of pathology indicates that both hypoxia and anoxia had occurred in the present cases.

Term monkey fetus 1620 sustained 50 min of rapidly developing severe asphyxia which began immediately after its in utero version. The arterial blood pO2 decreased from a normal value of 34 to 11-12 mm Hg while the blood pH fell from 7.35 to 6.70. During this asphyxia, hemoglobin-oxygen saturations below 5% were recorded. The complete collapse of the umbilical circulation several minutes prior to the reoxygenation of the fetus added an episode of total asphyxia. With reoxygenation following delivery, fetal cardiovascular performance improved rapidly though over an hour was required for recovery from the severe acidosis. The animal prospered but was found moribund on the 13th postnatal day due to dehydration. Brain examination after euthanasia revealed severe paracentral cortical and basal ganglia damage. Damage also appeared symmetrically in nuclei in the lower brain stem and in thalamus. These three zones of injury are attributed to the partial, the partial combined with the total, and the total asphyxia, respectively. The present case makes clear that compression of the umbilical cord may cause damage of a variety of types depending on the severity and duration of the asphyxia induced. It also demonstrates the possibility of recovery from a systemic acidosis where the pH values have fallen to levels below 6.70 for up to an hour.

Three groups of pregnant Wistar rats were subjected to 3 different levels of hypoxia: 11.6, 10.7 and 9.0%, respectively. Pair-fed and ad libitum fed control groups were included to control for the reduced food intake due to hypoxia. Within the range studied, fetal body weights decreased with decreased oxygen availability. Liver weights were more, brain weights less markedly reduced than body weights. Pair-fed but normally oxygenated animals showed slight reductions in body and organ weights compared to ad libitum fed controls. The fetuses subjected to hypoxia showed a placental hypertrophy relative to their body weights, while the least hypoxic fetuses showed an absolute placental hypertrophy. Placenta-fetal body ratios that were 150% greater than those observed in control animals were documented. In contrast, the fetuses of food-deprived animals were associated with abnormally small placentas.

Newborn rhesus monkeys were used to investigate the relation between the duration of total asphyxia and the magnitude of the postasphyctic cerebral glycogen hyper-deposition response. The latter has been observed to occur following episodes of total asphyxia lasting 12.5 min and to be maximal at 12 h into the recovery period. The changes in glycogen contents of other vital organs were also studied. A minimum duration of 9 min of total asphyxia was required for the first elicitation of the cerebral glycogen hyperdeposition response. The magnitude of the response once elicited did not vary whatever the duration of the asphyxia beyond 9 and up to 30 min. During the actual episodes of total asphyxia, the glycogen content of the brain diminished more rapidly and completely than did that of kidney or heart. The hepatic, pulmonary and muscle glycogen contents did not change significantly either during asphyxia or during the recovery period.