Hypoxia sustained

Seizures, muscular hyperactivity, and rigidity may result in death. Seizures may cause pulmonary aspiration, hypoxia, and brain damage. Hyperthermia may result from sustained muscular hyperactivity and can lead to muscle breakdown and myoglobinuria, renal failure, lactic acidosis, and hyperkalemia. Drugs and poisons that often cause seizures include... 

Contrary to the above information, Hentschel et al. (2003) demonstrated that under 5 min hypoxic conditions (95% N2-5% C02) in vitro, selective activation of A3AR by a brief (5 min) application of IB-MECA, inhibits excitatory neurotransmission on cortical neurons. Such effect is blocked by the selective A3AR antagonist MRS 1220. These data indicate that A3AR may sustain inhibition of synaptic activity during hypoxia and therefore mediate neuroprotection. Furthermore, IB-MECA... 

In a first attempt at a synthesis of information in this research (Hochachka, 1986), a channel arrest component of a hypoxia tolerance theory postulated (i) that hypoxia tolerant cells would have an inherent low permeability (either low channel densities or low channel activities) and (ii) that they would sustain a further suppression of membrane permeability to ions when exposed to oxygen lack (further channel arrest by either suppression of channel densities or channel activities). Turtle liver cells display both of these characteristics (especially when compared to mammalian homologs) thus they clearly fit the classical definition of metabolic and channel arrest as two telling signatures of hypoxia tolerance. 

While rescue of protein synthesis in hypoxia sensitive mammalian cells does not seem feasible without oxygen, exactly such a rescue system seems available to hypoxia tolerant cells (Land and Hochachka, 1995). One underlying rescue mechanism appears to require the overproduction of key elongation factors such as EFla with sustained hypoxia, the latter is overexpressed and accumulates throughout the stress period. 

Morris, S., and J. Collaghan (1998). Respiratory and metabolic responses of the Australian yabby, Cherax destructor, to progressive and sustained environmental hypoxia. J. Comp. Physiol. B. 168 377-388. 

Rosenberger C, Goldfarb M, Shina A, Bachmann S, Frei L), Eckardt K-U, SchraderT, Rosen S, and Heyman SN. Evidence for Sustained Renal Hypoxia and Transient Hypoxia Adaptation in Experimental Rhabdomyolysis-induced Acute Kidney Injury. Nephrol Dial Transplant doi 10.1093/ndt/gfm808,2007. 

Cysteine proteases, called calpains, are known to be activated by sustained elevations in intracellular free calcium. Once activated, calpains degrade the cytoskeleton, transmitter and membrane channels, and metabolic enzymes (Hou and MacManus 2002 Mattson 2003 Nicholls 2004). Functionally, calpains have been characterized as pivotal mediators of both active necrotic cell death and PCD (Wang 2000) following cell-damaging stressors and insults such as soman exposure, excitotoxic challenges, toxins, free radicals, UV radiation, acute hypoxia, traumatic brain injury, cytokines, heat, and in chronic neurodegenerative conditions (Fischer et al. 1991 Caner et al. 

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