Biomedical subjects

Jan G Nijhuis

Publications and source records attributed to Jan G Nijhuis.

4 recordsLinked to original sources

PubMed2003

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.

Acid-Base Equilibrium↗

PubMed2002

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 <or= 7.00): glucose, lactate, pyruvate, hypoxanthine, alanine, beta-hydroxybutyrate, choline, creatine, myo-inositol, citrate, succinate, valine, and an unknown metabolite characterized by a resonance at 1.56 ppm in the proton nuclear magnetic resonance spectrum. Twenty-four hours after the hypoxic insult, myo-inositol was increased, and alanine was decreased 48 h after the hypoxic insult, both compared with control values. Choline levels in CSF had a linear relationship with arterial pH (r = 0.26, p < 0.005). During severe hypoxia, CSF levels of succinate and choline are increased. Increased CSF levels of succinate may indicate dysfunction of the mitochondrial respiratory chain, whereas elevated CSF choline levels may indicate disrupted cell membranes. The increase of the CSF myo-inositol level after 24 and 48 h may indicate osmolytic cell changes causing cell edema. Decreased alanine level may represent changes in the source of excitatory amino acid synthesis.

3-Hydroxybutyric Acid↗

PubMed2002

Longitudinal study of fetal body movements: nomograms, intrafetal consistency, and relationship with episodes of heart rate patterns a and B.

Our objective was to investigate the longitudinal development of incidence parameters of fetal body movements to define normal reference ranges, to relate them to episodes of fetal heart rate patterns A and B, and to determine the intrafetal consistency for these parameters. Twenty-nine fetuses were studied longitudinally from 24 wk of gestation. Fetal body movements and heart rate were recorded at fortnightly intervals between 24 and 36 wk of gestation and weekly from 36 wk of gestation. Data were analyzed using multilevel analysis. Reference ranges were constructed for the percentage of observation time that movements were present, the number of movement bursts per hour, the mean burst duration, and the median onset-onset interval. The median percentage incidence of fetal body movements decreased from 17% at 24 wk to about 7% near term. The developmental course was the same during active episodes. Body movements also decreased during episodes of relative quiescence, in the course of pregnancy. Intrafetal variance was on average 40-80% of the total range of the four movement parameters. Normal reference ranges were developed for incidence parameters of fetal body movements from 24 wk of gestation onward. The overall decline in the incidence of movements during pregnancy appeared to be a developmental phenomenon and not due to progressively increasing episodes of fetal quiescence. Individual fetuses showed a degree of consistency in the percentage incidence of body movements, but intra- and interfetal variances were generally high, resulting in wide ranges.

Female↗

PubMedDate not supplied

Fetal behavior.

Fetal behavior reflects the activity of the fetal central nervous system (CNS). Insight in fetal behavior is crucial for the understanding of normal fetal well-being and in the evaluation of the possibly compromised fetus. In order to recognize 'behavioral' patterns, linkage of variables (absence of movements, absence of eye movements, heart rate patterns) is obligatory. No single test can predict with certainty if the fetus is compromised and/or what the optimal timing is for the delivery. That is why the study of fetal behavior is very time-consuming. Development of more appropriate methods to analyze fetal behavior should have high priority in clinical perinatology.

Behavior↗