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Systemic hypoxia elevates skeletal muscle interstitial adenosine levels in humans
D A MacLean1, L I Sinoway, U Leuenberger
1Section of Cardiology, The Milton S. Hershey Medical Center, Pennsylvania State University, Hershey, PA, USA. dmaclean@med.hmc.psghs.edu
Circulation
|November 10, 1998
Summary
During acute systemic hypoxia, interstitial adenosine levels significantly increase in skeletal muscle, contributing to peripheral vasodilation. This study quantifies adenosine
Area of Science:
- Cardiovascular Physiology
- Exercise Physiology
- Metabolic Regulation
Background:
- Adenosine is a known vasodilator, increasing in cardiac tissue during hypoxia.
- The specific substances causing peripheral vasodilation in skeletal muscle during hypoxia remain unclear.
Purpose of the Study:
- To measure and quantify skeletal muscle interstitial adenosine concentrations during acute systemic hypoxia.
Main Methods:
- Microdialysis technique used with 4 probes in the vastus lateralis muscle of 6 healthy males.
- Systemic hypoxia induced by breathing 10.5% O2 in N2 for 30 minutes.
- Arterial oxygen saturation and forearm blood flow monitored.
Main Results:
- Hypoxia lowered arterial oxygen saturation from 96% to 74.9%.
- Forearm blood flow increased by 28% during hypoxia.
- Skeletal muscle interstitial adenosine increased from 0.44 µmol/L at baseline to 1.03 µmol/L and 0.85 µmol/L after 15 and 30 minutes of hypoxia, respectively (P<0.05).
Conclusions:
- Interstitial adenosine plays a significant role in stimulating peripheral vasodilation during acute systemic hypoxia.
- Findings support the hypothesis that adenosine mediates hypoxic vasodilation in skeletal muscle.
Keywords:
Non-programmatic