Delayed ("secondary") cerebral energy failure after acute hypoxia-ischemia in the newborn piglet: continuous 48-hour studies by phosphorus magnetic resonance spectroscopy

摘要: ABSTRACT: Phosphorus (31P) spectra from the brains of severely birth-asphyxiated human infants are commonly normal on first day life. Later, cerebral energy failure develops, which carries a serious prognosis. The main purpose this study was to test hypothesis that delayed (“secondary”) could be reproduced in newborn piglet after severe acute reversed hypoxicischemic insult. Twelve piglets were subjected temporary occlusion common carotid arteries and hypoxemia [mean arterial Po2 3.1 (SD 0.6) kPa]. Mean phosphocreatine concentration [PCr]/inorganic orthophosphate [Pi] decreased 1.40 0.29) 0.01 0.02), nucleotide triphosphate [NTP]/exchangeable phosphate pool [EPP] 0.19 0.02) 0.06 0.04) (p<0.001 for each decrease). On reperfusion reoxygenation brain, mean [PCr]/[Pi] [NTP]/[EPP] returned baseline. Observations continuing next 48 h showed again decreased, spite Po2, blood pressure, glucose, 0.62 0.61) at 24 (p<0.01) 0.49 0.37) (p<0.001). also but lesser degree. Intracellular pH remained unchanged. These findings appeared identical with those seen infants. No changes metabolite concentrations took place six control piglets. severity secondary failure, as judged by lowest recorded 24-48 h, directly related extent depletion, obtained time integral reduction (p<0.0001). This animal model may prove useful testing cerebroprotective strategies.