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The Impact of Acute Isocapnic Hypoxia on Reactive Hyperemia in Young, Healthy Humans
Author(s) -
Kelsch Elizabeth A,
Keller Joshua L,
Crecelius Anne R
Publication year - 2016
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.30.1_supplement.763.22
Subject(s) - reactive hyperemia , medicine , pulse oximetry , vasodilation , plethysmograph , anesthesia , hypoxia (environmental) , forearm , cardiology , chemistry , oxygen , surgery , organic chemistry
Acute hypoxic exposure results in a number of significant physiological responses, including vasodilation in vascular beds of the skeletal muscle. The objective of this study was to investigate the effects of acute hypoxic exposure on microvascular function in young healthy humans, as determined by reactive hyperemia (RH). We first hypothesized that brief exposure to isocapnic hypoxia just prior to arterial occlusion would exaggerate the reactive hyperemic response, given hypoxic vasodilation may cause an increased oxygen mismatch. Second, we hypothesized continuous isocapnic hypoxia prior to and throughout arterial occlusion would attenuate the reactive hyperemic response given chronic exposure has been linked to vascular dysfunction. We tested subjects between the ages of 20 and 23 (n=6) with three counterbalanced trials: control, prior hypoxic exposure, and prolonged hypoxic exposure. Subjects were monitored for end‐tidal CO 2 (gas analyzer), O 2 saturation (pulse oximetry), heart rate (ECG) and blood pressure (sphygmomanometry). Forearm blood flow (FBF) measurements using venous occlusion plethysmography were made prior to and following 5 minutes of forearm ischemia (RH). During experimental trials, subjects breathed hypoxic gas to decrease arterial O 2 saturation to ~85% and isocapnia was maintained via a rebreathe system. Peak RH FBF was slightly increased after brief hypoxic exposure compared to normoxia (43.2±4.2 vs 40.3±6.2 ml/dl/min). However, in continuous hypoxia, peak RH FBF (39.6±3.9 ml/dl/min) was similar to normoxia. The total area under the curve during RH was similar in all three trials (normoxia: 156±9 ml; brief: 152±6 ml; continuous: 154±14 ml). Continuous hypoxia resulted in increased heart rate as compared to brief hypoxia and normoxia. The present results suggest that a brief period of hypoxia prior to occlusion does not impair RH responses. In addition, in young healthy humans, RH responses are preserved following continuous hypoxia throughout occlusion. Support or Funding Information University of Dayton‐ Research Council Grant‐In‐Aid; University Honors Berry Summer Thesis Program