國立臺灣大學醫學院外科簡雄飛2006-07-262018-07-112006-07-262018-07-112002-12-31http://ntur.lib.ntu.edu.tw//handle/246246/24470肌肉缺血再灌流傷害會造成肌肉移植後肌肉功能 不全或因血管阻塞後再灌流造成compartment syndrome。再灌流本身可能比缺血的傷害還大，這 是因缺血時所產生的xanthine oxidase, 再灌流後在 有氧的情況下代謝ATP 分解產物xanthine 與 hypoxanthine，產生氧自由基，雖然一些去氧自由 基的藥物如superoxide dismutase 及allopurinol 可減 緩一些傷害，但研究者相信中性球粘黏於血管壁， 在缺血處產生更多的氧自由基及傷害，是此病態生 理中重要的過程。我們在大鼠大腿處以tourniquet 造成4 小時缺血，再以in vivo MCLA 冷光測定儀 測定不同時間再灌流所造成oxygen free radicals (ORF)量，發現所測得最高量在第二天，此時以抗 中性球抗體(MCA967)染出最高量的中性球數，以 及以TUNEL 染出最多的肌肉細胞凋亡。故我們應 尋求較長期(>2d)有效的ORF 清除劑，尤其是中性 球的聚集因子(chemokine)的去除，才可有效的避免 肌肉缺血再灌流傷害，目前初步資料顯示，以抗體 阻斷聚集因子的確可減少中性球浸潤及ORF 產生。We studied the ischemia reperfusion injury of skeletal muscleby oxygen free radicals (OFRs) detection with MCLA chemiluminescence, neutrophil staining and TUNEL. The OFRs as well as neutrophils and muscle cell apoptosis peaked by day 2 after release of tourniquet. These findings are interesting because the neutrophil number and the muscle cells showing apoptosis are also peaking on day 2. Neutrophils are likely the major source of free radicals. The real-time oxygen free radical monitoring in the reperfused skeletal muscle was shown peaked on the 2nd day. This piece of information is important since the regimen decreasing the OFRs must be prolonged after 2nd day. Otherwise the clinical result must be poor. The source of this OFR was under investigated by neutrophil staining and real-time PCR of CINC(the chemokine for neutrophils of rats), which were shown to be correlated. Besides, the blocking antibodies to CINC could effectively decrease neutrophil infiltration and OFRs. However the data was only preliminary.application/pdf1217953 bytesapplication/pdfzh-TW國立臺灣大學醫學院外科muscleoxygen free radicalsischemia reperfusion injuryreporthttp://ntur.lib.ntu.edu.tw/bitstream/246246/24470/1/902314B002411.pdf