Systemic hypoxia elevates skeletal muscle interstitial adenosine levels in humans

Research output: Contribution to journalArticle

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Abstract

Background - Adenosine is a potent vasodilator that has been shown to increase in cardiac tissue in response to hypoxia. However, peripheral vasodilatation also occurs during hypoxia, and the vasoactive substance(s) responsible for skeletal muscle vasodilation have not yet been completely identified. Therefore, the purpose of this study was to measure and quantify skeletal muscle interstitial adenosine during acute systemic hypoxia. Methods and Results - Skeletal muscle interstitial adenosine concentrations were determined by the microdialysis technique, in which 4 semipermeable microdialysis probes were inserted into the vastus lateralis muscle of 6 healthy male subjects and perfused at a rate of 5 μL/min with Ringer's solution. Sixty minutes after the insertion of the microdialysis probes, systemic hypoxia was induced for 30 minutes by having the subjects breathe a mixture of 10.5% O2 in N2. Arterial oxygen saturation (fingertip oximeter) was lowered (P<0.05) from 96±0.7% to 74.9±1.4%, and forearm blood flow was increased 28%. During normoxia, the interstitial adenosine concentration was 0.44±0.08 μmol/L, and it was increased to 1.03±0.15 (P<0.05) and 0.85±0.09 (P<0.05) after 15 and 30 minutes of hypoxia, respectively. Conclusions - These data are consistent with the concept that during acute systemic hypoxia, interstitial adenosine plays a key role in stimulating peripheral vasodilation.

Original languageEnglish (US)
Pages (from-to)1990-1992
Number of pages3
JournalCirculation
Volume98
Issue number19
DOIs
StatePublished - Nov 10 1998

Fingerprint

Adenosine
Skeletal Muscle
Microdialysis
Vasodilation
Quadriceps Muscle
Vasodilator Agents
Forearm
Hypoxia
Healthy Volunteers
Oxygen
Muscles

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

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title = "Systemic hypoxia elevates skeletal muscle interstitial adenosine levels in humans",
abstract = "Background - Adenosine is a potent vasodilator that has been shown to increase in cardiac tissue in response to hypoxia. However, peripheral vasodilatation also occurs during hypoxia, and the vasoactive substance(s) responsible for skeletal muscle vasodilation have not yet been completely identified. Therefore, the purpose of this study was to measure and quantify skeletal muscle interstitial adenosine during acute systemic hypoxia. Methods and Results - Skeletal muscle interstitial adenosine concentrations were determined by the microdialysis technique, in which 4 semipermeable microdialysis probes were inserted into the vastus lateralis muscle of 6 healthy male subjects and perfused at a rate of 5 μL/min with Ringer's solution. Sixty minutes after the insertion of the microdialysis probes, systemic hypoxia was induced for 30 minutes by having the subjects breathe a mixture of 10.5{\%} O2 in N2. Arterial oxygen saturation (fingertip oximeter) was lowered (P<0.05) from 96±0.7{\%} to 74.9±1.4{\%}, and forearm blood flow was increased 28{\%}. During normoxia, the interstitial adenosine concentration was 0.44±0.08 μmol/L, and it was increased to 1.03±0.15 (P<0.05) and 0.85±0.09 (P<0.05) after 15 and 30 minutes of hypoxia, respectively. Conclusions - These data are consistent with the concept that during acute systemic hypoxia, interstitial adenosine plays a key role in stimulating peripheral vasodilation.",
author = "MacLean, {Dave A.} and Lawrence Sinoway and Urs Leuenberger",
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Systemic hypoxia elevates skeletal muscle interstitial adenosine levels in humans. / MacLean, Dave A.; Sinoway, Lawrence; Leuenberger, Urs.

In: Circulation, Vol. 98, No. 19, 10.11.1998, p. 1990-1992.

Research output: Contribution to journalArticle

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T1 - Systemic hypoxia elevates skeletal muscle interstitial adenosine levels in humans

AU - MacLean, Dave A.

AU - Sinoway, Lawrence

AU - Leuenberger, Urs

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N2 - Background - Adenosine is a potent vasodilator that has been shown to increase in cardiac tissue in response to hypoxia. However, peripheral vasodilatation also occurs during hypoxia, and the vasoactive substance(s) responsible for skeletal muscle vasodilation have not yet been completely identified. Therefore, the purpose of this study was to measure and quantify skeletal muscle interstitial adenosine during acute systemic hypoxia. Methods and Results - Skeletal muscle interstitial adenosine concentrations were determined by the microdialysis technique, in which 4 semipermeable microdialysis probes were inserted into the vastus lateralis muscle of 6 healthy male subjects and perfused at a rate of 5 μL/min with Ringer's solution. Sixty minutes after the insertion of the microdialysis probes, systemic hypoxia was induced for 30 minutes by having the subjects breathe a mixture of 10.5% O2 in N2. Arterial oxygen saturation (fingertip oximeter) was lowered (P<0.05) from 96±0.7% to 74.9±1.4%, and forearm blood flow was increased 28%. During normoxia, the interstitial adenosine concentration was 0.44±0.08 μmol/L, and it was increased to 1.03±0.15 (P<0.05) and 0.85±0.09 (P<0.05) after 15 and 30 minutes of hypoxia, respectively. Conclusions - These data are consistent with the concept that during acute systemic hypoxia, interstitial adenosine plays a key role in stimulating peripheral vasodilation.

AB - Background - Adenosine is a potent vasodilator that has been shown to increase in cardiac tissue in response to hypoxia. However, peripheral vasodilatation also occurs during hypoxia, and the vasoactive substance(s) responsible for skeletal muscle vasodilation have not yet been completely identified. Therefore, the purpose of this study was to measure and quantify skeletal muscle interstitial adenosine during acute systemic hypoxia. Methods and Results - Skeletal muscle interstitial adenosine concentrations were determined by the microdialysis technique, in which 4 semipermeable microdialysis probes were inserted into the vastus lateralis muscle of 6 healthy male subjects and perfused at a rate of 5 μL/min with Ringer's solution. Sixty minutes after the insertion of the microdialysis probes, systemic hypoxia was induced for 30 minutes by having the subjects breathe a mixture of 10.5% O2 in N2. Arterial oxygen saturation (fingertip oximeter) was lowered (P<0.05) from 96±0.7% to 74.9±1.4%, and forearm blood flow was increased 28%. During normoxia, the interstitial adenosine concentration was 0.44±0.08 μmol/L, and it was increased to 1.03±0.15 (P<0.05) and 0.85±0.09 (P<0.05) after 15 and 30 minutes of hypoxia, respectively. Conclusions - These data are consistent with the concept that during acute systemic hypoxia, interstitial adenosine plays a key role in stimulating peripheral vasodilation.

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