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Supramaximal Intensity Hypoxic Exercise and Vascular Function Assessment in Mice
Published on: March 15, 2019
Systemic hypoxia causes cutaneous vasodilation in healthy humans.
Grant H Simmons1, Christopher T Minson, Jean-Luc Cracowski
1Department of Human Physiology, University of Oregon, Eugene, OR 97403-1240, USA.
Hypoxia and hypercapnia cause vasodilation in skin blood vessels. This response is not limited by sympathetic vasoconstriction during hypoxia but may be influenced by it during hypercapnia.
Area of Science:
- Physiology
- Cardiovascular Science
- Thermoregulation
Background:
- Hypoxia and hypercapnia pose challenges to homeostasis by affecting sympathetic outflow and vascular smooth muscle.
- Cutaneous vasculature changes significantly impact blood pressure regulation and thermoregulation.
- Limited knowledge exists on how hypoxia and hypercapnia influence skin circulation.
Purpose of the Study:
- To investigate the effects of hypoxia and hypercapnia on cutaneous vascular conductance (CVC) in healthy subjects.
- To determine if adrenergic vasoconstriction modulates the vascular responses to hypoxia and hypercapnia in the skin.
Main Methods:
- 35 healthy subjects were studied using microdialysis fibers in the ventral forearm.
- One site was perfused with saline (control), and the other with bretylium tosylate to block sympathetic vasoconstriction.
- Skin blood flow was measured using laser-Doppler flowmetry, and CVC was calculated.
Main Results:
- Isocapnic hypoxia increased CVC in both control and bretylium-perfused sites, indicating vasodilation.
- Hyperpnea did not alter CVC.
- Hypercapnia increased CVC in the control site but not in the bretylium-perfused site, suggesting a role for adrenergic mechanisms.
Conclusions:
- Both hypoxia and hypercapnia induce modest vasodilation in nonacral skin.
- Neural adrenergic vasoconstriction does not impede hypoxic vasodilation.
- Adrenergic vasoconstriction may play a role in modulating hypercapnic vasodilation.
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