Hypoxia consequences

Chesney, Jr., E.J., and Baltz, D.M. (2001) The effects of hypoxia on the northern Gulf of Mexico coastal ecosystem a fisheries perspective. In Coastal hypoxia Consequences for Living Resources and Ecosystems (Rabalais, N.N., and Turner, R.E., eds.), pp. 321-354, Coastal and Estuarine Studies 58, American Geophysical Union, Washington, DC. 

Figure 4 Progressive changes in fish and invertebrate fauna as oxygen concentration decreases from 2mgl to anoxia. From Rabalais NN, Harper DE, Jr., and Tuner RE (2001) Responses of nekton and demersal and benthic fauna to decreasing oxygen concentrations. In Rabalais NN and Turner RE (eds.) Coastal and Estuarine Studies 58 Coastal Hypoxia Consequences for Living Resources and Ecosystems, pp. 115-128. Washington, DC American Geophysical Union.

Rabalais NN and Turner RE (eds.) (2001) Coastal and Estuarine Studies 58 Coastal Hypoxia - Consequences for Living Resources and Ecosystems. Washington, DC American Geophysical Union. 

State of deviation of plasma pH (systemic acidosis) or tissue extracellular pH (tissue or local acidosis) from normal (ca. pH 7.4) towards lower values. Deviation of 0.1 pH units is significant. Systemic acidosis can be caused by lung or kidney failure. Local acidosis can be the consequence of injury, inflammation, or tumor growth, due to disruption of blood supply. Local acidosis is normally associated with hypoxia. 

Inhalant intoxication dehrium can occur as a consequence of disturbances in dopaminergic, glutamatergic, and GABAergic neu to transmission secondary to acute, high-level exposure to psychoactive ingredients in solvents such as toluene, trichloroethane, and trichloroethylene. Systemic effects of solvent inhalation such as cerebral hypoxia and/or metabolic acidosis may also be involved (Rosenberg 1982). Under these circumstances, inhalant intoxication dehrium develops over a short period of time (usually hours to days) and tends to fluctuate during the course of the day. Usually, the delirium resolves as the intoxication ends or within a few hours after cessation of use. 

The principal function of the circulatory system is to supply oxygen and vital metabolic substrates to cells throughout the body, as well as removal of metabolic waste products. Circulatory shock is a life-threatening condition whereby this principal function is compromised. When circulatory shock is caused by a severe loss of blood volume or body water it is called hypovolemic shock, the focus of this chapter. Regardless of etiology, the most distinctive manifestations of hypovolemic shock are arterial hypotension and metabolic acidosis. Metabolic acidosis is a consequence of an accumulation of lactic acid resulting from tissue hypoxia and anaerobic... 

Lactic acidosis, which typically accompanies hypovolemic shock as a consequence of tissue hypoxia, is best treated by reversal of the underlying cause. Administration of alkalizing agents such as sodium bicarbonate has not been demonstrated to have any... 

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

As the AO with a direct nonspecific mechanism of action we have chosen Hypoxene - sodium poly(2,5-dihydroxiphenyl)-4-thiosulfonate. Besides a direct AO effect as a scavenger of free radicals it exerts an anti-hypoxic effect shunting I and II complexes of mitochondrial respiratory chain, which are inhibited as a consequence of hypoxia (Eropkin et al., 2007). Hypoxene was introduced into cell incubation media before illumination and left during cells further incubation. Hypoxene in the concentration of 40pg/ml, comparable to doses applied in vivo, completely blocked C60-induced phototoxicity (Table 7.3). Cellular viability has completely recovered to control level, which is a convincing evidence of free radical nature of cellular damage in photodynamic effect of fullerene. 

Taken together, these results showed that EGb can prevent ischemia-induced Na,K-AIPase injury, and suppress hypoxia- and ECS-induced membrane phospholipid breakdown in the brain, and bilobalide might be associated with its protective action. In addition, EGb reduces AA-induced neuronal damage as a consequence of the increase in reincorporation of AA Therefore, these mechanisms might provide a possible explanation for neuroprotective properties of EGb and bilobalide against oxidative damage. 

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