|Budget Amount *help
¥2,000,000 (Direct Cost : ¥2,000,000)
Fiscal Year 1992 : ¥700,000 (Direct Cost : ¥700,000)
Fiscal Year 1991 : ¥1,300,000 (Direct Cost : ¥1,300,000)
1. Cerebral energy metabolism in newborn mice was investigated during and after 8-hour hypoxia produced by exposure to a 5% oxygen, 95% nitrogen mixture by 31P magnetic resonance spectroscopy. PCr/Pi ratio decreased from a control value of 1.55 to 0.56 at the end of hypoxia. The brain intracellular pH (pHi) increased from 7.20 to 7.36 within 1 hour and stayed higher than control throughout the hypoxic period. The control value of mixed arterial and venous blood pH (pHb) was 7.39. pHb decreased immediately after the induction of hypoxia and fell to 7.16 at the end of hypoxia. These results suggest that there may be an unknown protective system in neonatal brain against systemic acidosis.
2. The effects of hypercapnic acidosis on neuronal activity and mitochondrial respiration were studied in the neonatal canin brain with EEG and 31P-MRS. Inspired CO2 levels of 13, 20, and 30% were administered through a ventilator and resulted in 3 levels of hypercapnia where measured PaCO2 values were approximately 70, 100, 140mmHg. pHi was reduced from 7.11 to 6.99, 6.87, and 6.76 in response to the increasing levels of hypercapnia, and free ADP decreased from 21.5 to 18.1, 14.8 and 12.9uM. The cerebral electrical activity was reduced by 20, 30, and 40%. The change in ADP concentration with respect to EEG output was fitted with the Michaelis-Menten relationship for the mitochondrial oxidative phosphorylative enzymes. This study provides evidence that free ADP regulates mitochondrial respiration during hypercapnic acidosis and that acidosis does not inhibit the mitochondrial substrate regulation of respiration.