phosphocreatine and Fetal-Hypoxia

Our purpose was to investigate the effect of hypoxia on calcium (Ca(++)) influx and Ca(++)-calmodulin (CaM)-dependent protein kinase IV (CaM kinase IV) activity in the neuronal nuclei of the guinea pig fetal cerebral cortex during development.. Preterm and term pregnant guinea pigs (n = 61) were exposed to either 21% or 7% oxygen for 60 minutes. Hypoxia in the fetal cerebral cortical tissue was documented by determining the tissue concentrations of adenosine triphosphate (ATP) and phosphocreatine. Fetal cerebral cortical neuronal nuclei were isolated and purified, and ATP-dependent Ca(++) influx and CaM kinase activity were determined.. Hypoxia resulted in increased neuronal intranuclear (45)Ca(++) influx for 2 minutes from 6.65 +/- 1.29 pmol/mg protein to 9.07 +/- 1.98 pmol/mg protein (P <.05) in preterm and from 6.65 +/- 1.63 pmol/mg protein to 11.26 +/- 1.79 pmol/mg protein (P <.05) in term fetuses. The hypoxia-induced (45)Ca(++) influx was significantly higher (P <.05) in the term than in the preterm fetuses. Hypoxia resulted in increased CaM kinase IV activity from 383.7 +/- 53.3 pmol/mg/min protein to 451.6 +/- 59.5 pmol/mg/min protein (P <.05) in the preterm and from 364.6 +/- 109.7 pmol/mg/min protein to 487.0 +/- 43.3 pmol/mg/min protein (P < 0.05) in term fetuses. No significant difference was observed in CaM kinase IV activity between the preterm and the term groups.. Cerebral hypoxia increases calcium influx and CaM kinase IV activity in the cortical neuronal nuclei of the guinea pig fetal brain during development.

Topics: Adenosine Triphosphate; Animals; Brain Chemistry; Calcium; Calcium-Calmodulin-Dependent Protein Kinases; Cerebral Cortex; Embryonic and Fetal Development; Female; Fetal Hypoxia; Neurons; Oxygen; Phosphocreatine; Pregnancy; Swine

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

Topics: Adenosine Triphosphate; Birth Injuries; Brain; Brain Damage, Chronic; Female; Fetal Hypoxia; Gangliosides; Histocytochemistry; Humans; Infant, Newborn; Lipid Metabolism; Lysosomes; Mitochondria; Oxygen Consumption; Phosphocreatine; Pregnancy; Time Factors