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Re-establishment of normal blood flow is mandatory to restore intramuscular high energy phosphate levels after transient ischemia
BMC Pharmacology volume 8, Article number: A52 (2008)
Background
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.
Methods
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).
Results
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.
Discussion
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.
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Open Access This article is published under license to BioMed Central Ltd. This is an Open Access article is distributed under the terms of the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/2.0 ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Andreas, M., Schmid, A.I., Doberer, D. et al. Re-establishment of normal blood flow is mandatory to restore intramuscular high energy phosphate levels after transient ischemia. BMC Pharmacol 8 (Suppl 1), A52 (2008). https://doi.org/10.1186/1471-2210-8-S1-A52
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DOI: https://doi.org/10.1186/1471-2210-8-S1-A52