Titlebook: Hypoxia and the Circulation; Robert C. Roach (Research Director),Peter D. Wagne Conference proceedings 2007 The Editor(s) (if applicable)

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Victor D. Köchli,Borut Marinceked epidemiologic studies have shown associations, often independent of obesity, between SA (or surrogates such as snoring) and measures of glucose dysregulation or type 2 diabetes. However, treatment of SA with continuous positive airway pressure (CPAP) has not been conclusive in demonstrating impro

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https://doi.org/10.1007/978-3-662-13435-1s are also present. Thus, oxidant stress and inflammation are potential mediators of intermittent hypoxia-induced vascular dysfunction. Once the mechanisms of intermittent hypoxia-induced alterations in vascular structure and function are understood, strategies can be developed to reverse or prevent

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https://doi.org/10.1007/978-3-642-41616-3tion of RAS is especially important because it can lead to constriction of efferent arterioles, hypoperfusion of postglomerular peritubular capillaries, and subsequent hypoxia of the tubulointerstitium in the downstream compartment. Recent studies using BOLD-MRI showed an immediate decrease of oxyge

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https://doi.org/10.1007/978-3-662-65850-5 uteroplacental environment will vary with gestational age and will depend on the extent of trophoblast invasion and artery remodelling. Fluctuations in oxygen tension may be an important determinant of cellular events both during invasion towards uterine vessels and during the remodelling process.

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https://doi.org/10.1007/978-3-642-99067-0al bronchiolitis) and reactive species (in acute lung injury). Finally, βadrenergic agonists have been shown experimentally to reverse defects in ENaC function, and improve hypoxemia and pulmonary edema, and may provide a novel therapeutic modality for ARDS, although some viral lung pathogens appear

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https://doi.org/10.1007/978-3-658-40045-3lular matrix thanks to the mechanical role of matrix chondroitin sulphate proteoglycans (CS-PGs). This increase in pressure buffers microvascular filtration. Hypoxia causes fragmentation of CS-PGs of the extracellular matrix and of HS-PGs of the basement membrane: the result is a decrease in tissue

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https://doi.org/10.1007/978-90-313-7191-4s mediated by the generation of mitochondrial reactive oxygen species (ROS) as shown by pharmacological and genetic approaches. Hypoxia and ROS promote the PKC-zeta dependent phosphorylation of the Na,K-ATPase alpha subunit triggering its endocytosis in a clathrin–AP2 dependent process. The phosphor

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https://doi.org/10.1007/978-3-662-64621-2s (e.g. the mole rat Spalax and goldfish) express more Ngb in their brains than their oxygen-deprivation sensitive relatives. These data suggest that Ngb may have a myoglobin-like role and supplies oxygen to the respiratory chain of the metabolically highly active neurons, or protect them from react