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Abstract #1069

Effects from inhalation of hypoxic air and carbon monoxide exposure on human cerebral perfusion, oxygen consumption and lactate production

Mark Bitsch Vestergaard1, Hashmat Ghanizada2, Ulrich Lindberg1, Nanna Arngrim2, Olaf Paulson3, Messoud Ashina2, and Henrik Bo Wiberg Larsson1
1Functional Imaging Unit, Department of Clinical Physiology, Nuclear Medicine and PET, Copenhagen University Hospital Rigshospitalet, Glostrup, Denmark, 2Danish Headache Center, Department of Neurology., Copenhagen University Hospital Rigshospitalet, Glostrup, Denmark, 3Neurobiology Research Unit, Department of Neurology, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark

In present study we demonstrate that in healthy humans the cerebral lactate concentration increases during inhalation of hypoxic air but not after exposure to carbon monoxide. This suggests a regulatory mechanism of cerebral glycolytic activity possibly mediated by sensing of arterial oxygen pressure and that the lactate production is not solely a result of hindered oxidative metabolism, at least during non-threatening hypoxic exposure. Phase-contrast mapping and susceptibility-based oximetry were used to acquire global cerebral blood flow and oxygen consumption and MR-spectroscopy was used to measure the lactate concentration in the occipital lope in a total of 51 healthy humans.

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