Hypoxia oxygen exposure

Fig. 2.1 Glucose and ketone body transporters with hypoxia. The relative increase in moncar-boxylate (MCTl) and glucose (GLUTl) transporters at the blood—brain barrier following 10% (0.5 atm. oxygen) exposure of hypobaric-hypoxia. Quantification of cerebral capillary density, as measured by GLUTl immunostaining, and MCTl immunoreactivities (number of counts per mm ) showed about a 30% upregulation of MCT 1 and GLUTl transporters with 3 week hypoxic exposure in rat brain. P < 0.05, hypoxic vs. normoxic...

Bilberg and collaborators studied the effects of sUver nanoparticies on the breathing of the Eurasian perch. The final results revealed that exposure to silver nanoparticies reduced tolerance to hypoxia (oxygen deficiency) (Bilberg et al., 2010). 

It is known that the endothelial cells lining the capillary bed are markedly damaged during hyperoxic exposure. However, it is not at present known whether this damage is due to free-radical-induced injury of the endothelial cells or whether endothelial cells are simply responding to the diminished blood flow produced by the severe vasoconstriction. The theoretical basis for free-radical involvement is sound and it has been proposed that low oxygen tensions (hypoxia) followed by periods of reoxygenation are the most likely explanation for the disorder (Kelly, 1993). 

Holland et al. [125] have shown that the potent vascular smooth muscle cell mitogen and phospholipase A2 activator thrombin stimulated superoxide production in human endothelial cells, which was inhibited by the NADPH oxidase inhibitors. Similarly, thrombin enhanced the production of oxygen species and the expression of )Alphos and Rac2 subunits of NADPH oxidase in VSMCs [126,127]. Greene et al. [128] demonstrated that the activator of NO synthase neuropeptide bradykinin is also able to stimulate NADPH oxidase in VSMCs. Similar to XO, NADPH oxidase enhanced superoxide production in pulmonary artery smooth muscle cells upon exposure to hypoxia [129]. 

Until recent times, the only toxicological hazards attributable to nitrous oxide were those common to asphyxiants, with death or permanent brain injury occurring only under conditions of hypoxia. A number of untoward and toxic effects have now been associated with exposure. One of the earliest findings was that patients given 50% nitrous oxide and 50% oxygen for prolonged periods, to induce continuous sedation, developed bone marrow depression and granuloqn openia. The bone marrow usually returned to normal within a matter of days once the nitrous oxide was removed, but several deaths from aplastic anemia have been recorded. ... 

Administration of hyperbaric oxygen following exposure to carbon tetrachloride improved survival from 31 to 96% in rats (Ellenhorn and Barceloux 1988). Hyperbaric oxygen has also been used in treating overdoses of carbon tetrachloride in humans and may correct regional tissue hypoxia and damage, as well as inhibit the P-450-dependent reductive dehalogentation of carbon tetrachloride to the metabolically active acute trichloromethyl radical in the liver. However, the effectiveness of this method has not been established in humans (Burkhart et al. 1991 Ellenhorn and Barceloux 1988). 

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