Müller M, Schmid R, Nieszpaur-Los M, Fassolt A, Lönnroth P, Fasching P, Eichler H G
Department of Clinical Pharmacology, University of Vienna, Austria.
Eur J Clin Invest. 1995 Aug;25(8):601-7. doi: 10.1111/j.1365-2362.1995.tb01752.x.
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 +/- 0.6 mM; 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), TxB2 (n = 6) and urea (n = 8) were characterized during a 20 min period of leg constriction. TxB2 increased exclusively during reperfusion in comparison to baseline (n = 6). Administration of 500 mg acetylsalicylic acid, 5-10 min after onset of ischaemia blunted TxB2-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 TxB2 is not evident during ischaemia. TxB2 mediated reperfusion injury might be reduced by acetylsalicylic acid, even if administered after onset of ischaemia.
通过微透析研究了缺血及缺血后组织损伤关键代谢产物在人骨骼肌细胞间空间的组织动力学。体内微透析校准实验（n = 5）得出人骨骼肌细胞间葡萄糖的基础浓度（3.6±0.6 mM；平均值±标准差）。相应的平均血浆葡萄糖浓度为4.3±0.2 mM，显著更高。在腿部收缩20分钟期间，对细胞间葡萄糖（n = 7）、乳酸（n = 5）、血栓素B2（TxB2，n = 6）和尿素（n = 8）的时间-浓度曲线进行了表征。与基线相比（n = 6），TxB2仅在再灌注期间增加。缺血开始后5 - 10分钟给予500 mg阿司匹林可减弱TxB2对再灌注的反应（n = 4）。得出的结论是，细胞间肌肉葡萄糖浓度低于血浆中的浓度。即使在缺血条件下，骨骼肌对葡萄糖的摄取也很快。缺血期间TxB2的合成和释放不明显。阿司匹林可能会减轻TxB2介导的再灌注损伤，即使在缺血开始后给药也是如此。
