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Key metabolite kinetics in human skeletal muscle during ischaemia and reperfusion: measurement by microdialysis
Author(s) -
MÜLLER M.,
SCHMID R.,
NIESZPAURLOS M.,
FASSOLT A.,
LÖNNROTH P.,
FASCHING P.,
EICHLER H. G.
Publication year - 1995
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1995.tb01752.x
Subject(s) - microdialysis , skeletal muscle , medicine , chemistry , metabolite , ischemia , extracellular , glucose uptake , endocrinology , intracellular , perfusion , extracellular fluid , biochemistry , insulin
. The tissue kinetics of key metabolites of ischaemic and postischaemic tissue damage were studied in the intercellular space of human skeletal muscle by microdialysis. In vivo microdialysis calibration experiments ( n = 5) yielded the basal intercellular concentration of glucose in human skeletal muscle (3.6±0.6mM; mean±SD). The corresponding mean plasma glucose concentration was 4.3 ± 0.2 mM which was significantly higher. The time vs. concentration profiles of intercellular glucose ( n = 7), lactate ( n = 5), TxB 2 ( n = 6) and urea ( n = 8) were characterized during a 20 min period of leg constriction. TxB 2 increased exclusively during reperfusion in comparison to baseline ( n = 6). Administration of 500 mg acetylsalicylic acid, 5–10min after onset of ischaemia blunted TxB 2 ‐response to reperfusion ( n = 4). It is concluded that intercellular muscle glucose concentration is less than that in plasma. Glucose uptake in skeletal muscle is rapid even under ischaemic conditions. Synthesis and release of TxB 2 is not evident during ischaemia. TxB 2 mediated reperfusion injury might be reduced by acetylsalicylic acid, even if administered after onset of ischaemia.