Ikezawa T
First Department of Surgery, Nagoya University School of Medicine, Japan.
Nihon Geka Gakkai Zasshi. 1989 Oct;90(10):1799-805.
Twenty adult mongrel dogs were divided into three groups. Group I: control (n = 7), group II: limb ischemia for 6 hours followed by reperfusion (n = 6), and group III: administration of alpha-tocopherol after 6 hours of ischemia, and reperfusion (n = 7). In group II, serum CPK and LPO increased after reperfusion with peak levels of 38,000 +/- 9,800 mU/ml and 20.4 +/- 3.7 nmol/ml respectively, which were significantly higher than those in group I. (CPK: p less than 0.02, LPO less than 0.03). In group III, the peak levels of serum CPK and LPO were regulated to the low level of 1,060 +/- 290 mU/ml and 9.2 +/- 4.5nmol/ml, respectively, which were significantly lower than those in group II. (CPK: p less than 0.02, LPO less than 0.04). Additional 13 dogs were divided into two groups in order to assess tissue LPO in the limb, liver, and kidney. Group A: control (n = 5), group B: reperfusion after 6 hours of ischemia (n = 8). Tissue LPO level of 1.89 +/- 0.74nmol/mg-protein in the gastrocnemius muscle in group B was significantly higher than that in group A (p less than 0.02), although there was no significant difference in the gracilis muscle, liver, and kidney. These results prove indirectly the participation of lipid peroxidative reaction by active oxygen in the mechanism of development of reperfusion injury, and suggest the preventive effect of alpha-tocopherol to reperfusion injury.
20只成年杂种犬被分为三组。第一组：对照组（n = 7）；第二组：肢体缺血6小时后再灌注（n = 6）；第三组：缺血6小时后给予α-生育酚并再灌注（n = 7）。在第二组中，再灌注后血清肌酸磷酸激酶（CPK）和脂质过氧化产物（LPO）升高，峰值水平分别为38,000±9,800 mU/ml和20.4±3.7 nmol/ml，显著高于第一组（CPK：p<0.02，LPO<0.03）。在第三组中，血清CPK和LPO的峰值水平分别调节至较低水平，即1,060±290 mU/ml和9.2±4.5 nmol/ml，显著低于第二组（CPK：p<0.02，LPO<0.04）。另外13只犬被分为两组以评估肢体、肝脏和肾脏中的组织LPO。A组：对照组（n = 5）；B组：缺血6小时后再灌注（n = 8）。B组腓肠肌中的组织LPO水平为1.89±0.74 nmol/mg蛋白，显著高于A组（p<0.02），尽管股薄肌、肝脏和肾脏中无显著差异。这些结果间接证明了活性氧引发的脂质过氧化反应参与了再灌注损伤的发生机制，并提示α-生育酚对再灌注损伤具有预防作用。
