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Re-establishment of normal blood flow is mandatory to restore intramuscular high energy phosphate levels after transient ischemia

  • Martin Andreas1,
  • Albrecht I Schmid2,
  • Daniel Doberer1,
  • Martin Meyerspeer2,
  • Ewald Moser2,
  • Michael Roden3 and
  • Michael Wolzt1Email author
BMC Pharmacology20088(Suppl 1):A52

Published: 5 November 2008


Blood FlowIschemiaGastrocnemius MuscleHealthy Male SubjectTransient Ischemia


Normalization of blood flow is required to salvage ischemic tissues, but might paradoxically cause reperfusion injury. The aim of this study was to determine whether restoration of skeletal muscle high energy phosphates after ischemia is affected by post-ischemic vessel stenosis.


Leg ischemia was induced by a cuff on one thigh for 20 minutes and muscle high energy phosphates depleted by lower leg exercise (n = 5 healthy male subjects). After calf ischemia, the cuff was either deflated or air pressure maintained at 20 mmHg below systolic pressure for 5 min (stenosis). Measurements of high-energy phosphates in gastrocnemius muscle were performed with a 3 T spectrometer. 31P and 1H spectra were acquired as an estimate of myocellular concentrations of phosphocreatine (PCr) and inorganic phosphate (iP).


PCr concentrations decreased to 31% ± 16% during ischemic exercise (p < 0.001) and iP levels increased in parallel. While PCr re-established within 2 min after cuff deflation, no recovery was detectable when blood flow was impaired in the reperfusion phase.


Muscle phosphate recovery depends on normalization of blood flow. These data indicate that intensified strategies to re-establish flow conditions are required for residual myocellular function after transient ischemia.

Authors’ Affiliations

Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria
MR Center of Excellence, Center for Biomedical Engineering and Physics, Medical University of Vienna, Vienna, Austria
Department of Internal Medicine, Heinrich Heine University, Düsseldorf, Germany


© Andreas et al; licensee BioMed Central Ltd. 2008

This article is published under license to BioMed Central Ltd.