Correlation between cerebral energy metabolism using ^<31>P-NMR and cerebral blood flow : Pathophisiological studies on hypoxic-ischemic encephalopathy in newborn piglets

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For the pathophysiological study of hypoxic-ischemic encephalopathy, using the experimental condition of 15 min of graded hypoxia, we measured cerebral energy metabolism using phosphorus 31 nuclear magnetic resonanse spectroscopy (<@D131@>D1P-NMR) and cerebral blood flow (total CBF) with colored microspheres in seven newborn piglets within 24 hours after birth, which resemble human newborns in terms of cerebral growth. Total CBF before hypoxic insulte (control) was 50.2(]SY.+-。[)6.5 ml/min/100g. At 15 minutes after the start of hypoxic insulte (FiO<@D22@>D2=0.08), CBF increased to 90.1(]SY.+-。[)19.1ml/min/100g and became 1.8 times as much as the control. However, at 45 minutes after hypoxia (FiO<@D22@>D2=0.05), total CBF decreased to 42.2(]SY.+-。[)12.0 ml/min/100g and no significant difference was found compared to control. With regards to bradycardia (HR<100), total CBF was significantly decreased to 18.3(]SY.+-。[)9.4 ml/min/100g. On brain stem (pons, mid brain and medulla), blood flow was significantly increased at 45minutes, too, and was not significantly decreased on bradycardia. Compared to total CBF,considerably more blood flow was measured at 45 minutes and on bradycardia.There was a significant correlation between mean arterial blood pressure (MABP) and CBF (r=0.861, P<0.001). The autoregulation of total CBF was proved to be disturved. The Phosphocreatinine (PCr) /inorganic phosphate (Pi) and intracellular pH (pHi) did no change until total CBF reached levels below the levels control. The PCr/Pi and pHi suddenly decreased when total CBF decreased below the control. There was a significant correlation between total CBF and the PCr/Pi or pHi (r=0.843, p<0.001 and r=0.796, P<0.001). There was no significant correlation between PaO_2 and the PCr/Pi.Therefore, these results suggest that CBF is the most important factor in maintaining cerebral energy metabolism on hypoxic-ischemic encephalopathy.