Hypoxia-ischemia energy failure

Energy failure, an early consequence of hypoxia-ischemia, causes disruption of ionic homeostasis and accumulation of extracellular neurotransmitters 559... 

A. Lorek, Y. Takei, E. B. Cady, J. S. Wyatt, J. Penrice, A. D. Edwards, D. Peebles, M. Wylezinska, H. Owen-Reece V. Kirkbride, et al.. Delayed (secondary) cerebral energy failure after acute hypoxia-ischemia in the newborn piglet continuous 48-hour studies by phosphorus magnetic resonance spectroscopy. Pediatr. Res., 1994, 36, 699-706. 

R. C. Vannucci, J. Towfighi and S. J. Vannucci, Secondary energy failure after cerebral hypoxia-ischemia in the immature rat. J. Cereb. Blood Flow Metab., 2004, 24,1090-1097. 

Y. S. Chang, W. S. Park, M. Lee, K. S. Kim, S. M. Shin, and J. H. Choi, Near-Infrared Spectroscopic Monitoring of Secondary Cerebral Energy Failure after Transient Global Hypoxia-Ischemia in the Newborn Piglet, Neurological Res., 21(2), 216-224 (1999). 

Alteration in mental status occurring in patients with systanic sepsis always carries a serious prognosis. The mechanisms of impaired brain function are poorly understood and are probably multifactorial. Considerations include hypoxia, ischemia, mitochondrial dysfunction and anaerobic cerebral energy metabolism, blood-brain barrier dysfunction or impaired transporter function, cerebral edema, toxins like ammonia or endotoxins, and last but not least, clinical use of cerebral depressants and sedatives in severely ill patients. In patients with multi-organ failure, clearance of common short-acting sedatives can become prolonged, resulting in severe and protracted alteration of mentation. 

In infants who have suffered perinatal hypoxic-ischaemic brain injury (birth asphyxia), P spectra obtained within a few hours of birth show no abnormalities. However, in many cases a delayed secondary energy failure (SEP) develops within 24 h. The Pi signal increases, accompanied by reduced PCr and, in severe cases, low NTP. Furthermore, in contrast to the profound acidosis seen during acute hypoxia-ischemia, an intracellular alkalosis may be detected. Additionally, localized spectroscopy shows elevated lactate levels for several weeks following SEE. Both PCr/Pi and lactate/N-acetylaspartate (Lac/NAA) ratios have proved to be extremely useful indices of the severity of hypoxic-ischaemic injury, with strong prognostic capabilities. 

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