phosphocreatine and Fetal-Growth-Retardation

To examine the sensitivity of proton MR spectroscopy for detecting early central nervous system abnormalities in neonates born to human immunodeficiency virus (HIV)-positive mothers.. Asleep, unsedated, and continuously monitored by electrocardiography, 10 newborns, 5 with HIV-positive and 5 with HIV-negative mothers, were studied within the first 10 days of life in a 1.5-T scanner. After T1- and T2-weighted images were obtained, proton spectra were performed using voxels of interest (3.4 cm3) in the deep parietooccipital white matter. Peaks were identified as N-acetyl-aspartate (2.0 ppm), creatine and phosphocreatine (3.0 ppm), choline (3.2 ppm), and inositol (3.5 ppm). Peak areas were used to calculate metabolic ratios: N-acetyl-aspartate to creatine, inositol to creatine, and creatine to choline.. All newborns of HIV-positive mothers had abnormal proton spectra compared with control infants; a nonspecific amino acid peak in the 2.1- to 2.6-ppm area was elevated, broad, and overlapping the N-acetyl-aspartate peak in all the HIV-exposed newborns and in only 1 of the 5 control newborns. The choline-to-creatine ratio was higher in HIV-exposed newborns at 2.3 +/- 0.4 (normal term, 0.9 +/- 0.3), as was the N-acetyl-aspartate-to-creatine ratio at 2.6 +/- 0.9 (for control subjects, 1.2 +/- 0.4). MR images from these brain regions were all considered normal. Because acquired immunodeficiency syndrome develops in only a small fraction of neonates born to HIV-seropositive mothers, the above spectral abnormalities found in all our subjects may result from indirect effects of HIV, such as intrauterine growth retardation.. These findings indicate that proton MR spectroscopy might play an important role in detecting early central nervous system complications in newborns of HIV-seropositive mothers.

Topics: AIDS Dementia Complex; Aspartic Acid; Choline; Diagnosis, Differential; Energy Metabolism; Female; Fetal Growth Retardation; HIV Seropositivity; Humans; Infant, Newborn; Infectious Disease Transmission, Vertical; Inositol; Magnetic Resonance Imaging; Magnetic Resonance Spectroscopy; Male; Occipital Lobe; Parietal Lobe; Phosphocreatine

31-P magnetic resonance spectroscopy (MRS) allows noninvasive measurements of cerebral phosphorus compounds: ATP, phosphocreatine (PCr), inorganic phosphate (Pi), phosphomonoesters (PME) and phosphodiesters (PDE). In this paper we reported our MRS data from the brains of infants with intrauterine growth retardation, respiratory distress syndrome, neonatal seizures or neonatal asphyxia, and discussed the possibilities to prevent brain damage due to these perinatal troubles.

Topics: Adenosine Triphosphate; Asphyxia; Brain; Energy Metabolism; Fetal Growth Retardation; Humans; Infant, Newborn; Magnetic Resonance Spectroscopy; Phosphocreatine; Respiratory Distress Syndrome, Newborn; Seizures

Cerebral oxidative metabolism during intrauterine growth retardation was investigated utilizing a pregnant-rat model. Dams were subjected to unilateral uterine artery ligation on the 17th day of gestation. At term, they were sacrificed by decapitation and the fetuses delivered by cesarean section. Body and brain weights of fetuses from ligated uterine segments were smaller than those of offspring from nonligated horns of the experimental rats or those from sham-operated dams. Blood glucose at birth was reduced by 25% in growth-retarded fetuses. Cerebral oxidative metabolites, including glycogen, glucose, lactate, ATP, and phosphocreatine, were not different from control levels. These findings suggest that neither tissue hypoxia nor deficient glucose delivery to brain can account for the stunted cerebral growth observed in fetuses following uterine artery ligation.

Topics: Adenosine Triphosphate; Animals; Body Weight; Brain; Female; Fetal Growth Retardation; Fetal Hypoxia; Glucose; Glycogen; Lactates; Organ Size; Oxygen Consumption; Phosphocreatine; Pregnancy; Rats