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The sympathetic chemoreflex response to hypoxia in humans is sensitised by prior exposure to 8 h of isocapnic hypoxia
Author(s) -
Croft Quentin,
Sander Mikael,
MacDonald Ian,
Simpson Liz,
Dorrington Keith,
Robbins Peter
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.1008.14
Subject(s) - microneurography , hypoxia (environmental) , medicine , heart rate , anesthesia , sympathetic nervous system , sympathetic activity , chemoreceptor , ventilation (architecture) , cardiology , baroreflex , blood pressure , oxygen , chemistry , receptor , organic chemistry , mechanical engineering , engineering
In healthy humans the ventilatory sensitivity to acute hypoxia is increased by prior exposure to hypoxia for 8 h. Here we test the hypothesis that the sympathetic chemoreflex is similarly sensitised by a prior short‐term exposure to hypoxia. Healthy humans (n=9) were exposed to eucapnic hypoxia (controlled end‐expiratory PO 2 = 45 mmHg) for 10 minutes before and after 8 h in an hypoxic chamber (controlled end‐expiratory PO 2 = 50 mmHg). Muscle sympathetic nervous activity (MSNA) was determined by peroneal microneurography (morning recording in one leg and evening recording from the contralateral leg). Acute hypoxic exposure before vs after the chamber resulted in oxygen desaturation (arterial saturations 82±1 vs 81±1 %) and increases in heart rate (+15±2 vs +20±1 b·min‐1), ventilation (+8±1 vs +20±1 l·min‐1), and MSNA (+61±14 vs +154±34 % total activity), all p<0.05. These results demonstrate robust sensitization of sympathetic as well as ventilatory chemoreflexes in healthy humans following an 8‐h exposure to mild hypoxia. This work was supported by The Wellcome Trust and University College, Oxford.