| Autor: |
Mattos JD; Laboratory of Exercise Sciences, Fluminense Federal University, Niterói, Brazil., Campos MO; Laboratory of Exercise Sciences, Fluminense Federal University, Niterói, Brazil., Rocha MP; Laboratory of Exercise Sciences, Fluminense Federal University, Niterói, Brazil., Mansur DE; Laboratory of Exercise Sciences, Fluminense Federal University, Niterói, Brazil., Rocha HNM; Laboratory of Exercise Sciences, Fluminense Federal University, Niterói, Brazil., Garcia VP; Laboratory of Exercise Sciences, Fluminense Federal University, Niterói, Brazil., Rocha NG; Laboratory of Exercise Sciences, Fluminense Federal University, Niterói, Brazil., Alvares TS; Nutrition Institute, Federal University of Rio de Janeiro, Macaé, Brazil., Secher NH; Department of Anesthesia, The Copenhagen Muscle Research Centre, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark., Nóbrega ACL; Laboratory of Exercise Sciences, Fluminense Federal University, Niterói, Brazil., Fernandes IA; NeuroV̇ASQ̇-Integrative Physiology Laboratory, Faculty of Physical Education, University of Brasília, Brasília, Brazil. |
| Abstrakt: |
Isocapnic hyperoxia (IH) evokes cerebral and peripheral hypoperfusion via both disturbance of redox homeostasis and reduction in nitric oxide (NO) bioavailability. However, it is not clear whether the magnitude of the vasomotor responses depends on the vessel network exposed to IH. To test the hypothesis that the magnitude of IH-induced reduction in peripheral blood flow (BF) may differ from the hypoperfusion response observed in the cerebral vascular network under oxygen-enriched conditions, nine healthy men (25 ± 3 yr, mean ± SD) underwent 10 min of IH during either saline or vitamin C (3 g) infusion, separately. Femoral artery (FA), internal carotid artery (ICA), and vertebral artery (VA) BF (Doppler ultrasound), as well as arterial oxidant (8-isoprostane), antioxidant [ascorbic acid (AA)], and NO bioavailability (nitrite) markers were simultaneously measured. IH increased 8-isoprostane levels and reduced nitrite levels; these responses were followed by a reduction in both FA BF and ICA BF, whereas VA BF did not change. Absolute and relative reductions in FA BF were greater than IH-induced changes in ICA and VA perfusion. Vitamin C infusion increased arterial AA levels and abolished the IH-induced increase in 8-isoprostane levels and reduction in nitrite levels. Whereas ICA and VA BF did not change during the vitamin C-IH trial, FA perfusion increased and reached similar levels to those observed during normoxia with saline infusion. Therefore, the magnitude of IH-induced reduction in femoral blood flow is greater than that observed in the vessel network of the brain, which might involve the determinant contribution that NO has in the regulation of peripheral vascular perfusion. |
