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Cerebral function in the growth-retarded fetus and neonate
I Kjellmer1, M Thordstein, M Wennergren
1Department of Pediatrics, University of Göteborg, Sweden.
Insights
Fetal growth retardation in neonates (small for gestational age) is linked to neurological issues and heightened vulnerability to oxygen deprivation. Studies show altered brain function and metabolism in growth-restricted fetuses, increasing risks.
Area of Science:
- Neuroscience
- Developmental Biology
- Perinatology
Background:
- Intrauterine growth retardation (IUGR) is a known risk factor for permanent neurological disabilities in newborns.
- The precise mechanisms linking fetal growth restriction to brain dysfunction and hypoxia vulnerability remain incompletely understood.
Purpose of the Study:
- To investigate if fetal growth retardation causes primary brain development perturbations.
- To determine if growth-restricted fetuses exhibit increased vulnerability to hypoxic events.
Main Methods:
- Evoked potentials were assessed in small for gestational age (SGA) neonates and compared to controls.
- Experimental models in guinea pigs and rats were used to induce growth retardation by reducing placental blood flow.
- Brain monoamine metabolism, aspartate levels, and lipid peroxidation were analyzed under normoxic and hypoxic conditions.
Main Results:
- SGA neonates showed a high frequency of abnormal evoked potentials with significantly longer latencies.
- Growth-retarded guinea pups had impaired somatosensory evoked responses during hypoxia.
- Growth-retarded rat fetuses displayed altered serotonin metabolism and lower aspartate levels.
- Increased lipid peroxidation was observed in growth-retarded fetuses during hypoxia.
Conclusions:
- Fetal growth retardation is associated with primary alterations in brain function and development.
- Growth-restricted fetuses exhibit increased vulnerability to hypoxic stress, indicated by impaired neural responses and biochemical changes.
- These findings highlight the neurodevelopmental risks associated with IUGR and its impact on brain resilience to oxygen deprivation.
Abstract:
Intrauterine growth retardation is associated with increased risks for permanent neurological disabilities. A series of studies was undertaken to elucidate whether fetal growth retardation causes a primary perturbation of brain function and development and whether an increased vulnerability for periods of oxygen lack exists. In two groups of neonates who were small for gestational age (SGA) evoked potentials were investigated. A high frequency of abnormal recordings were obtained in SGA babies. SGA babies had significantly longer latency periods for the primary evoked potentials than appropriately grown controls. In guinea pigs and rats growth retardation was induced by reducing the placental blood flow during late gestation. Growth retarded guinea pups demonstrated a considerable reduction of the ability to retain normal somatosensory evoked response during hypoxia compared to appropriately grown littermates. Growth retarded rat fetuses exhibited marked changes of the monoamine metabolism in the brain inasmuch as basal levels of serotonin and its main metabolite were low while an inappropriate acceleration of the serotonin synthesis rate took place during hypoxia. The tissue concentrations of aspartate were also significantly lower in growth retarded fetuses than normally grown littermates. Finally, lipid peroxidation was assessed. During adequate oxygenation no difference was observed when lipid peroxidation was assessed. During adequate oxygenation no difference was observed when lipid peroxidation in brain tissue of growth retarded and appropriately grown fetuses was compared but during mild-moderate hypoxia lipid peroxidation was significantly more intense in the growth retarded group.(ABSTRACT TRUNCATED AT 250 WORDS)