Titlebook: Hypoxia; Into the Next Millen Robert C. Roach,Peter D. Wagner,Peter H. Hackett Book 1999 The Editor(s) (if applicable) and The Author(s), u

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Wie KI das Marketing neu definiert responses which act to preserve the fetal oxygen supply. The fetus also utilizes several compensatory mechanisms to survive brief periods of hypoxia. While fetal heart rate monitoring data during air travel suggest no compromise of fetal oxygenation, exercise at high altitude may place further stre

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https://doi.org/10.1007/978-3-658-20819-6APE. Although high pulmonary artery pressure appears to be a condition ‘sine qua non’ it is not clear what causes the exaggerated pressure response and how it accounts for the leak. Animal models and findings in bronchoalveolar lavage fluid indicate a role for increased permeability due to inflammat

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https://doi.org/10.1007/978-3-8349-4296-8duals AMS may progress to a lethal form of HACE and/or high-altitude pulmonary edema (3). Two hypotheses have been promulgated to account for HACE: the vasogenic edema hypothesis and the cytotoxic edema hypothesis (3,4). Since cerebral energetics are unchanged during AMS-HACE in an experimental shee

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https://doi.org/10.1007/978-3-658-26763-6le compounds under physiological conditions. Under pathological conditions such as trauma or ischemia, BBB permeability may increase thus allowing plasma constituents to escape into brain tissue. This “opening” of the BBB may, at least in part, be mediated by massive release of autacoids resulting i