Failure energy

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

Pannunzio, P., Hazell, A. S., Pannunzio, M., Rama Rao, K. V. and Butterworth, R. F. Thiamine deficiency results in metabolic acidosis and energy failure in cerebellar granule cells an in vitro model for the study of cell death mechanisms in Wernicke s encephalopathy. /. Neurosci. Res. 62 286-292, 2000. 

Inner membrane damage, permeabihty transition (PT) pore opening, energy failure, apoptosis, apo-necrosis, cytotoxicity... 

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. 

K. Kawada, M. Namba, T. Nishida T. Imai, et al.. Relationship between cerebral oxygenation and phosphorylation potential during secondary energy failure in hypoxic-ischemic newborn piglets. Pediatr. Res., 2009,65, 317-322. 

If we do not use our own coal and uranium to their maximum potential, then we do so at our peril because we cannot exist as as industrial nation. There simply is not enough petroleum and natural gas to give us the equivalent energy. Failure to recognize this vital fact will lead us to our inevitable doom. An enlightened leader can prevent us from becoming a satellite of the Middle East or a fourth rate power. 

Especially in models of transient cerebral ischemia, apoptotic cell death has been observed after 3-7 days post insult in selected brain regions in which basal energy metabolism has been preserved (Chen et al. 1997 Du et al. 1996). In the meantime, molecular switches have been identified that gate different populations of neurons with regard to the type of cell death they eventually undergo (Nicotera 2003). However, there is little doubt that in animal stroke the vast majority of cells would die from necrosis or, alternatively, secondary energy failure even in the presence of a pro-apop-totic genetic balance. The concept of thresholds of cerebral blood flow (CBF) for various functions of brain parenchyma (see below) explains why the infarct core suffers from pan-necrosis whereas the peri-infarct border in which function is suppressed, but structure initially preserved (the so-called ischemic penumbra), may show apoptotic cell death or a combination of both. 

Besides the variable functional outcome after ischemia in animal models, it is well established that specific neuronal populations within an individual vary substantially in ischemic tolerance. Neurons in the CA1 region of the hippocampus and other distinct cellular populations of the caudate, thalamus, neocortex and cerebellum are selectively vulnerable to relatively brief periods of ischemia (Kirino and Sano 1984 Siesjo 1988). The reasons for this phenomenon are not fully elucidated, but for example in cerebellar Purkinje cells it could be shown that a reduced level of aldolase may trigger energy failure after brief periods of anoxia (Welsh et al. 2002). Changes in microcirculation, as seen in focal stroke,... 

Busza AL, Allen KL, King MD, van Bruggen N, Williams SR, Gadian DG (1992) Diffusion-weighted imaging studies of cerebral ischemia in gerbils potential relevance to energy failure. Stroke 23 1602-1612... 

Pathophysiologically, the pronounced ADC decline during ischemia occurs at the same time as anoxic depolarization. Anoxic depolarization is the consequence of energy failure with secondary failure of ion pumps (in particular Na+/K+-ATPase), which are necessary to maintain ion gradients over cell membranes. The resulting influx of Na+-ions is accompanied by a water shift from the extra- to the intracellular space (cytotoxic edema) without a net uptake of water (Fig. 7.1). 

While this association between the ischemia-associated ADC decline and energy failure/anoxic depolarization is undisputed, it is still a matter of debate what exactly leads to the restriction in water proton diffusion. As already mentioned above, water... 

Fig. 7.1. Pathophysiology of abnormal diffusion in cerebral ischemia. Cascade of metabolic changes leading to a decrease in diffusion of water protons in cerebral ischemia. The main steps leading to significant diffusion reductions are shown, while modest changes may also be found with incomplete energy failure. [Reproduced with permission from Neumann-Haefelin and Moseley (2003)]...

Lian, X.Y., Stringer, J.L. (2004). Energy failure in astrocytes increases the vulnerability of neurons to spreading depression. Eur. J. Neurosci. 19 2446-54. 

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