Vitamin A status after prophylactic intramuscular vitamin A supplementation in extremely low birth weight infants.

Background: Vitamin A supplementation (VAS) is recommended to prevent bronchopulmonary dysplasia (BPD). Our objective was to evaluate the effect of VAS on vitamin A (VA) status. We hypothesized that VAS would improve VA status in extremely low birth weight (ELBW) infants.

Adult responses to an ischemic stroke in a rat model of neonatal stress and morphine treatment.

Critically ill newborn infants experience stressors that may alter brain development. Using a rodent model, we previously showed that neonatal stress, morphine, and stress plus morphine treatments each influence early gene expression and may impair neurodevelopment and learning behavior. We hypothesized that the combination of neonatal stress with morphine may alter neonatal angiogenesis and/or adult cerebral blood vessel density and thus increase injury after cerebral ischemia in adulthood.

Long-term effects of neonatal stress on adult conditioned place preference (CPP) and hippocampal neurogenesis.

Critically ill preterm infants are often exposed to stressors that may affect neurodevelopment and behavior. We reported that exposure of neonatal mice to stressors or morphine produced impairment of adult morphine-rewarded conditioned place preference (CPP) and altered hippocampal gene expression. We now further this line of inquiry by examining both short- and long-term effects of neonatal stress and morphine treatment.

Left ventricular hypertrophy is prevalent in Sprague-Dawley rats.

Unrecognized cardiovascular abnormalities may confound the interpretation of research data collected using rats. However, although SPF rat colonies are screened for microbes and kept under standardized environmental conditions, their cardiovascular status is largely unknown. We recently performed surgery on anesthetized 80-d-old Sprague-Dawley rats and observed a high mortality that could not be attributed to the procedures or preceding treatments.

Rising prevalence of gastroschisis in Washington State.

The aim of this study was to assess gastroschisis prevalence in Washington (WA) State in relation to putative risk factors. Gastroschisis prevalence was calculated from the WA State birth cohort during 1987-2006 using an administrative database with birth certificate data linked with hospital discharge records and the ICD-9 procedure code 54.71, which specifies gastroschisis repair.

Effects of neonatal stress and morphine on murine hippocampal gene expression.

Critically ill preterm infants experience multiple stressors while hospitalized. Morphine is commonly prescribed to ameliorate their pain and stress. We hypothesized that neonatal stress will have a dose-dependent effect on hippocampal gene expression, and these effects will be altered by morphine treatment.

Effects of neonatal stress and morphine on kappa opioid receptor signaling.

Background: Critically ill neonates experience multiple stressors during hospitalization. Opioids are commonly prescribed to ameliorate their pain and stress. However, the enduring effects of stress and opioids are not understood.

Neonatal stress or morphine treatment alters adult mouse conditioned place preference.

Background: Hospitalized preterm infants may experience pain and stress, and narcotics are often administered to lessen their suffering. However, prolonged narcotic therapy may be detrimental during neonatal brain development. Using a rat model combining neonatal stress and morphine, we found that neonatal morphine impaired adult learning.

A phase I/II trial of high-dose erythropoietin in extremely low birth weight infants: pharmacokinetics and safety.

Objectives: High-dose recombinant erythropoietin is neuroprotective in animal models of neonatal brain injury. Extremely low birth weight infants are at high risk for brain injury and neurodevelopmental problems and might benefit from recombinant erythropoietin. We designed a phase I/II trial to test the safety and determine the pharmacokinetics of high-dose recombinant erythropoietin in extremely low birth weight infants.

The effects of binge alcohol exposure in the 2nd trimester on the estimated density of cerebral microvessels in near-term fetal sheep.

Heavy fetal alcohol exposure is associated with a spectrum of neurological abnormalities, although the mechanism of injury is largely unknown. We previously reported attenuated cerebral blood flow response to hypoxia in fetal and newborn sheep which were exposed to alcohol earlier in pregnancy. One possible mechanism for this effect of alcohol on the developing cerebral vasculature is a decrease in cerebral microvessel density, similar to its effect on developing neurons.

Effects of binge alcohol exposure in the second trimester on intracerebral arteriolar function in third trimester fetal sheep.

Fetal alcohol syndrome is a leading cause of mental retardation, but mechanisms of alcohol-associated brain damage remain elusive. Chronic alcohol exposure attenuates fetal and neonatal hypoxic cerebral vasodilation in sheep. We therefore hypothesized that alcohol could alter development of cerebrovascular responses to adenosine, a putative mediator of hypoxic cerebral vasodilation.

The effect of binge fetal alcohol exposure on the number of vasoactive intestinal peptide-producing neurons in fetal sheep brain.

Previously we demonstrated that fetal alcohol exposure attenuates hypoxic cerebral vasodilation in fetal and neonatal sheep. One mechanism may be altered expression of brain vasoactive substances. We hypothesized that early fetal alcohol exposure alters the number of fetal neurons expressing vasoactive intestinal peptide (VIP), a potent cerebral vasodilator.

Fetal alcohol exposure alters cerebrovascular reactivity to vasoactive intestinal peptide in adult sheep.

Chronic fetal alcohol exposure impairs neural and vascular development. We have previously shown that fetal alcohol exposure is associated with attenuated hypoxic cerebral vasodilation and reduced neuronal vasoactive intestinal peptide (VIP) expression in fetal sheep. In the present study, we tested the hypothesis that fetal alcohol exposure alters vascular development, leading to altered cerebral vascular reactivity to VIP in adulthood.

Binge alcohol exposure in the second trimester attenuates fetal cerebral blood flow response to hypoxia.

Alcohol is detrimental to the developing brain and remains the leading cause of mental retardation in developed countries. The mechanism of alcohol brain damage remains elusive. Studies of neurological problems in adults have focused on alcohol's cerebrovascular effects, because alcoholism is a major risk factor for stroke and cerebrovascular injuries.

Dopamine does not limit fetal cerebrovascular responses to hypoxia.

Dopamine is used clinically to stabilize mean arterial blood pressure (MAP) in sick infants. One goal of this therapeutic intervention is to maintain adequate cerebral blood flow (CBF) and perfusion pressure. High-dose intravenous dopamine has been previously demonstrated to increase cerebrovascular resistance (CVR) in near-term fetal sheep.

Effects of first trimester binge alcohol exposure on developing white matter in fetal sheep.

Heavy prenatal alcohol exposure is associated with neurodevelopmental abnormalities. Neuropathologic and neuroimaging studies have shown a wide range of structural problems, including abnormal neuronal migration and volume reduction in specific brain regions, including white matter. We identified foci of significant fetal white matter microglia-macrophage immunoreactivity in a "binge" model of early prenatal alcohol exposure in sheep.

Preliminary evidence that prenatal alcohol damage may be visible in averaged ultrasound images of the neonatal human corpus callosum.

Brain damage consequent to prenatal alcohol exposure can be detected by measurements of the corpus callosum in the midline magnetic resonance (MR) brain image in adolescents and adults. The present article extends this finding into the neonatal period, when the power of detection to ameliorate the quality of the child's future life is greatest. The midline corpus callosum of the very young infant can be located reliably in multiple frames of clinical transfontanelle ultrasound.

Cerebrovascular effects of rapid volume expansion in preterm fetal sheep.

Preterm human infants are often treated with volume expansion during their initial stabilization. There are limited data regarding the cerebral vascular effects of this therapeutic approach. The effects of blood volume expansion on cerebral vascular reactivity and oxygen metabolism in very immature animals have not been determined.

Erytropoietin concentrations in cerebrospinal fluid of nonhuman primates and fetal sheep following high-dose recombinant erythropoietin.

Erythropoietin (Epo) decreases neuronal injury and cell death in vitro and in vivo. To lay the groundwork for use of Epo as a potential therapy for brain injury, we tested the hypothesis that systemic dosing of high-dose recombinant Epo (rEpo) would result in neuroprotective rEpo concentrations in the spinal fluid of adult and developing animals. This report characterizes the pharmacokinetics of high-dose rEpo in the blood and spinal fluid of juvenile and adult nonhuman primates (n = 7) and fetal sheep (n = 37) following a single injection.

Cerebrovascular effects of intravenous dopamine infusions in fetal sheep.

Preterm infants are often treated with intravenous dopamine to increase mean arterial blood pressure (MAP). However, there are few data regarding cerebrovascular responses of developing animals to dopamine infusions. We studied eight near-term and eight preterm chronically catheterized unanesthetized fetal sheep.