Cerebral Tolerance of Hypoxia in Growth-Retarded and Appropriately Grown Newborn Guinea Pigs

Abstract

ABSTRACT. To elucidate if there is a reduced perinatalPao2, oxygen tension of arterial blood tolerance of hypoxia in growth retardation and approach CMR02, cerebral metabolic rate of oxygen its pathophysiologic background, newborn guinea pigs of different weights were subjected to standardized hypoxia. Intrauterine growth retardation was induced through uterine artery ligation. After spontaneous delivery experiments were performed within 2 days. After stabilization, hypoxia of stepwise increased severity was instituted. Blood gases, metabolic, cardiovascular, and neurophysiologic [somatosensory-evoked potentials (SEP)] parameters were monitored. A control series in which equally large blood samples were taken at the same intervals was performed. The animals were grouped according to birth weight: 2101 g (n = 10,12), 71-100 g (n = 11, lo), and 570 g (n = 8,3) (hypoxic and control series, respectively). Basal SEP latencies did not differ between the groups. Under hypoxia, both the amplitude of the SEP and the time to complete loss of the SEP was reduced in proportion to the degree of growth retardation. The differences between all groups were significant. The animals in the control series did not change their SEP performance significantly. Slight differences in metabolic and cardiovascular parameters between the groups were found not likely to explain the differences in SEP performance. Therefore, it is concluded that a reduced cerebral tolerance of hypoxia prevails in growthretarded newborn guinea pigs and that this is related to changes in the brain itself. It is also concluded that a relations hi^ exists between the degree of growth retardation and tiat of reduced cerebral ~ypoxiautolerance. (Pediatr Res 24: 633-638, 1988) IUGR resulting in neonates who are SGA remains a major problem in modern perinatal care. Fetuses and neonates who are SGA are overrepresented in clinical materials of children with neurodevelopmental handicaps (1-5) and have a several-fold increased risk of perinatal asphyxia (6, 7) compared to fetuses and neonates who are AGA. It is uncertain if there is also a reduced tolerance of asphyxia in SGA individuals, the underlying pathophysiologic background of which is obscure. Possible explanations are disturbed metabolic (8, 9) or cardiovascular (10) function. Alterations indicating a change in central nervous function have also been noted, suggesting that the reason might reside in the brain itself (1 1-1 5).In countries where malnutrition is uncommon, the majority of IUGR cases is caused by various conditions leading to placental vascular insufficiency with impaired exchange of gases and nutrients over the placenta (16). The aim of this study was to monitor metabolic, cardiovascular, and cerebral function under standardized, progressive hypoxia in newborn guinea pigs with different degrees of IUGR, produced by placental vascular insufficiency. This would make it possible to investigate if there is a reduced perinatal tolerance of hypoxia in growth retarded individuals and if so, approach i...

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