Aspects of fetal learning and memory.

Ninety-three pregnant women were recruited to assess fetal learning and memory, based on habituation to repeated vibroacoustic stimulation of fetuses of 30-38 weeks gestational age (GA). Each habituation test was repeated 10 min later to estimate the fetal short-term memory. For Groups 30-36, both measurements were replicated in a second session at 38 weeks GA for the assessment of fetal long-term memory. Within the time frame considered, fetal learning appeared GA independent. Furthermore, fetuses were observed to have a short-term (10-min) memory from at least 30 weeks GA onward, which also appeared independent of fetal age. In addition, results indicated that 34-week-old fetuses are able to store information and retrieve it 4 weeks later.

The relation between venous reserve capacity and low plasma volume.

OBJECTIVE: Prepregnant low plasma volume (LPV) is associated with subsequent gestational hypertensive disease. It is unknown to what extent an LPV affects the venous reserve capacity (VRC). We tested the hypothesis that LPV reduces the VRC, as indicated by presyncope or altered cardiovascular changes in response to head-up tilt. STUDY DESIGN: In 52 nonpregnant women with a history of preeclampsia or recurrent miscarriage, the authors assessed plasma volume, stroke volume, and cardiac output and determined blood pressure, heart rate, and autonomic responses to stepwise inflicted head-up tilt. RESULTS: 12 participants had LPV, which related to presyncope when compared with subjects with normal plasma volume (NPV). Women with LPV without presyncope demonstrated a circulatory response comparable to NPV women at the expense of consistently higher heart rate. CONCLUSION: LPV decreases the capacity to cope with head-up tilt without affecting the response pattern, suggesting reduced VRC.

Cerebral (31)P magnetic resonance spectroscopy and systemic acid-base balance during hypoxia in fetal sheep.

The purpose of this study was to investigate cerebral energy metabolism and acid-base homeostasis during impaired oxygen supply in fetal sheep. Systemic acid-base balance was correlated with the sequence in changes of cerebral phosphorus metabolite ratios and intracellular pH. Phosphorus magnetic resonance spectra were obtained from the brain of six fetal sheep simultaneously with repeated measurements of fetal arterial oxygen saturation and acid-base balance. Fetal hypoxia was induced by gradually reducing the oxygen supply to the anesthetized pregnant ewe to establish an intended arterial pH of 7.00 or lower. The ratio of phosphocreatine to inorganic phosphate decreased from 1.08 +/- 0.10 (SD) during the control period to 0.77 +/- 0.29 at an arterial pH between 7.20 and 7.25. The inorganic phosphate level became significantly increased at an arterial pH between 7.10 and 7.15 compared with control values. With ongoing arterial acidosis, cerebral intracellular pH decreased linearly with the arterial pH. At an arterial pH of 7.00, cerebral intracellular pH was decreased from 7.18 +/- 0.03 to 6.71 +/- 0.28, and phosphocreatine and nucleoside triphosphates levels were decreased significantly. In fetal sheep brain, cerebral oxidative phosphorylation (ratio of phosphocreatine to inorganic phosphate) is already affected at a mild arterial acidosis. At an arterial pH of 7.00 or lower, nucleoside triphosphates disappeared, which almost inevitably was followed by death in fetal sheep.

1H-NMR spectroscopy of cerebrospinal fluid of fetal sheep during hypoxia-induced acidemia and recovery.

The purpose of the study was to investigate the sequence of processes occurring during and after hypoxia-induced acidemia. We used proton nuclear magnetic resonance spectroscopy, which provides an overview of metabolites in cerebrospinal fluid (CSF), reflecting neuronal metabolism and damage. The pathophysiological condition of acute fetal asphyxia was mimicked by reducing maternal uterine blood flow in 14 unanesthetized pregnant ewes. CSF metabolites were measured during hypoxia-induced acidemia, and during the following recovery period, including the periods at 24 and 48 h after the hypoxic insult. Maximum values of the following CSF metabolites were reached during severe hypoxia (pH