冠状动脉旁路移植术患者尿液氧化应激指标分析。

W B Gerritsen, L P Aarts, W J Morshuis, F J Haas
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引用次数: 14

摘要

对20例择期行冠状动脉旁路移植术患者尿液中氧化应激指标进行了测定。在尿液中测量次黄嘌呤、黄嘌呤和尿酸,作为缺血的标志物,同时测量丙二醛,这是脂质过氧化的标志物。为纠正冠状动脉旁路移植术中出现的肾功能不全,测定了尿、血浆肌酐浓度。术中血浆肌酐浓度明显升高,从84 +/- 23 mumol/l上升到133 +/- 52 mumol/l,而再灌注时尿肌酐浓度明显下降,从8.29 +/- 4.45 mmol/l下降到2.70 +/- 1.01 mmol/l。为了便于比较,尿液中观察到的测量值以每摩尔肌酐表示。再灌注时,次黄嘌呤和黄嘌呤的排泄量分别从麻醉诱导后的15.0 +/- 7.3和10.9 +/- 5.7 mmol/mol肌酐增加到33.1 +/- 16.7和17.4 +/- 11.1 mmol/mol肌酐。丙二醛排泄量明显增加,从麻醉诱导后的1.38 +/- 0.80 mmol/mol肌酐增加到再灌注时的最高3.87 +/- 1.87 mmol/mol肌酐。尿中的嘌呤和丙二醛(以肌酐的比值表示)在冠状动脉旁路移植术中由于氧介导的组织损伤而增加。
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Indices of oxidative stress in urine of patients undergoing coronary artery bypass grafting.

Indices of oxidative stress in urine were measured in twenty patients undergoing elective coronary artery bypass grafting. Hypoxanthine, xanthine and uric acid were measured in urine, as markers of ischaemia together with malondialdehyde, which is a marker for lipid peroxidation. To correct for renal dysfunction during coronary artery bypass grafting the creatinine concentration was measured in urine and plasma. The creatinine concentration in plasma increases significantly during surgery, from 84 +/- 23 mumol/l to 133 +/- 52 mumol/l, whereas the creatinine concentration in urine decreases significantly, from 8.29 +/- 4.45 mmol/l to 2.70 +/- 1.01 mmol/l, during reperfusion. For reasons of comparison, the values of the observed measurements in urine are expressed per mol creatinine. The hypoxanthine and xanthine excretions both increase significantly, from 15.0 +/- 7.3 and 10.9 +/- 5.7 mmol/mol creatinine, respectively, after induction of anaesthesia to a maximum of 33.1 +/- 16.7 and 17.4 +/- 11.1 mmol/mol creatinine, respectively, during reperfusion. The malondialdehyde excretion increases significantly, from 1.38 +/- 0.80 mmol/mol creatinine after induction of anaesthesia to a maximum of 3.87 +/- 1.87 mmol/mol creatinine during reperfusion. The purines and malondialdehyde in urine (expressed as a ratio of creatinine), increase during coronary artery bypass grafting as a consequence of oxygen mediated tissue injury.

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