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In the first few days of hypoxic exposure, left ventricular dysfunction is consistently observed in the human heart, yet the cellular mechanisms underlying the dysfunction are poorly understood.
Our hypothesis was that normobaric hypoxia impairs cardiac energetics, leading to cardiac dysfunction in healthy subjects.
Normal healthy volunteers underwent 20 h of normobaric hypoxia in purpose-built hypoxia chambers. The partial pressure of oxygen during end tidal expiration (PETO2) was kept between 50 and 60 mm Hg, while keeping peripheral oxygen saturation (SpO2) above 80%. Cardiac function was measured using magnetic resonance imaging and echocardiography. High-energy phosphate metabolism was measured as the ratio of phosphocreatine to ATP (PCr/ATP) by 31phosphorus magnetic resonance spectroscopy before and after 20 h of hypoxia. Healthy men (n=12, aged 24±2 years) were recruited from the University of Oxford.
During hypoxia, PETO2 and SpO2 averaged 55±1 mm Hg and 83.6±0.4%, respectively. There was a 15% reduction in cardiac PCr/ATP, from 2.0±0.1 to 1.7±0.1 after hypoxia (p<0.01) and reduced diastolic function, measured as E/E′, from 6.1±0.4 to 7.5±0.7, p<0.01.
Short-term normobaric hypoxia led to rapid changes in cardiac metabolism and alterations in diastolic function in normal human hearts. Impaired high-energy phosphate metabolism may explain the cardiac dysfunction observed after hypoxic exposure, whether in health or disease.
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