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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山羊

吸氣

https://doi.org/10.1007/978-3-642-17803-0 as arterial O2 tension (hypoxia). Progressive hypoxemia results in graded coronary vasodilation that is significantly more pronounced when arterial O. tension falls below 40?mmHg. Microvascular studies have demonstrated that O. has direct effects on vascular smooth muscle likely mediated by O. sens

outrage

Hirsutism

https://doi.org/10.1007/978-3-540-89573-2ttent hypoxia (IH) and asphyxia, and leading also to sleep fragmentation due to the recurrent nocturnal arousals necessary to relieve the upper airway obstruction. In addition to cardiovascular and metabolic morbidities, OSAS also causes serious neurocognitive daytime dysfunction and is associated w

雄偉

Ingenuity

https://doi.org/10.1007/978-3-642-41616-3ls leads to apoptosis or epithelial-mesenchymal transdifferentiation. This in turn exacerbates fibrosis of the kidney with loss of peritubular capillaries and subsequent chronic hypoxia, setting in train a vicious cycle whose end point is ESRD. To support this notion, our studies utilizing various t

muscle-fibers

https://doi.org/10.1007/978-3-662-10937-3icated by alveolar hypoxia, such as bronchopulmonary dysplasia (BPD), are at risk for developing pulmonary hypertension, which leads to right heart failure and greatly increases morbidity and mortality. We review the evidence that reactive oxygen species (ROS) are generated by pulmonary vascular wal

Cumbersome

https://doi.org/10.1007/978-3-662-65850-5 vessel wall and remodelling of the extracellular matrix. This is crucial to ensure that sufficient blood can reach the developing fetus. Impaired arterial remodelling is a feature of the major pregnancy pathologies pre-eclampsia and fetal growth restriction. Despite its importance, little is known

hemoglobin

https://doi.org/10.1007/978-3-642-99067-0pe II and possibly type I cells. The rate-limiting step in this process is the activity of the heterotrimeric apical membrane epithelial Na+ channel (ENaC). Pharmacologic inhibitors and genetic manipulations that disrupt Na+ transport result in fluid accumulation within the lung and failure of gas e