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The influence of growth retardation on perinatal hypoxic-ischemic brain damage
W H Trescher1, R A Lehman, R C Vannucci
1Department of Pediatrics (Pediatric Neurology), Milton S. Hershey Medical Center, Pennsylvania State University College of Medicine, Hershey 17033.
Insights
Nutritional deprivation in immature rats reduced their susceptibility to brain damage from hypoxia-ischemia. Well-nourished animals showed greater tissue injury, suggesting protection against hypoxic-ischemic brain damage.
Area of Science:
- Neuroscience
- Developmental Biology
- Perinatal Medicine
Background:
- Hypoxia-ischemia (HI) is a major cause of brain injury in newborns.
- Intrauterine growth retardation (IUGR) is associated with increased risk of adverse neurodevelopmental outcomes.
- The impact of nutritional status on HI brain injury susceptibility in immature brains is not fully understood.
Purpose of the Study:
- To investigate the effect of growth retardation on the extent of brain damage following hypoxia-ischemia in immature rats.
- To determine if nutritional deprivation influences susceptibility to HI-induced brain injury.
Main Methods:
- Immature rats were raised in large (14 pups) or small (6 pups) litters to induce growth retardation.
- On postnatal day 7, rats underwent unilateral common carotid artery ligation followed by 3 hours of hypoxia.
- Brain damage was assessed at 30 days of age by measuring cerebral hemisphere dimensions.
Main Results:
- Rats in larger litters (poorer nutrition) weighed significantly less than those in smaller litters.
- The extent of brain damage varied, with no significant difference in the range between well-nourished and poorly nourished groups.
- Significantly greater brain tissue injury was observed in well-nourished animals compared to poorly nourished ones (P = 0.003).
Conclusions:
- Nutritional deprivation in immature rats is associated with decreased susceptibility to hypoxia-ischemia brain damage.
- Findings suggest a protective effect of poor nutrition against HI-induced brain injury in the developing brain.
- Results have implications for understanding brain injury in human infants with intrauterine growth retardation (IUGR).
Abstract:
The effect of growth retardation on the extent of brain damage produced by hypoxia-ischemia was assessed in immature rats. Newborn rats were raised in litters of 6 or 14 pups from day 2 to 7. On postnatal day 7, those immature rats raised in litters of 14 weighed 18% less than animals raised in litters of 6 (P less than 0.001). They then were subjected to cerebral hypoxia-ischemia by unilateral common carotid artery ligation followed by 3 h of exposure to 8% oxygen-92% nitrogen at 37 degrees C. Upon return to their dams, all litters were culled to 6 pups. At 30 days of age, the animals underwent perfusion-fixation of their brains under pentobarbital anesthesia. Brain damage was assessed by measuring the length and width of each cerebral hemisphere. The extent of brain damage varied from no difference in the size of the two cerebral hemispheres to marked shrinkage of the hemisphere ipsilateral to the common carotid artery occlusion. The range of brain damage between the well-nourished and poorly nourished animals was comparable. Rank order of the extent of damage demonstrated significantly greater tissue injury in those animals well nourished prior to hypoxia-ischemia (Mann-Whitney U-test; P = 0.003). The results indicate that nutritional deprivation in the immature rat is associated with a decreased rather than increased susceptibility to brain damage arising from hypoxia-ischemia. The findings of the investigation have relevance to the human infant suffering from intrauterine growth retardation (IUGR).