目的：观察2型糖尿病（T2DM）下肢血管病变（PAD）患者下肢动脉介入治疗前后病变动脉血清中超氧化物歧化酶（SOD）水平的变化，探讨T2DM合并PAD患者体内氧化应激水平及介入治疗对血清SOD的影响。方法选择2011年7月-2012年12月接受介入治疗的T2DM合并PAD患者40例，其中下肢单纯动脉造影者（A组）16例，行下肢动脉造影、球囊扩张及支架植入者（B组）24例（Fontaine分期Ⅱb期和Ⅲ期的患者）。B组中，单纯行下肢动脉造影、球囊扩张者16例（B1组），行下肢动脉造影、球囊扩张且行支架植入者8例（B2组）。门诊健康体检者（C组）20名作为对照组。A、B两组介入术前行常规检查并取静脉血测血脂、糖化血红蛋白（HbA1c）和SOD水平。 C组在同样条件下抽取肘静脉血测定上述指标。A、B两组术中取介入前动脉血，术后24 h取静脉血测定各组血清SOD水平。结果 A组患者下肢动脉造影无明显狭窄。 A、B、C 3组SOD分别为（46.1±3.13）u/ml，（35.37±3.58）u/ml，（60.50±6.99）u/ml， A、B组SOD水平均明显低于C组（t=8.420，P＜0.01；t=14.324，P＜0.01），A组SOD水平明显高于B组（t=10.092，P＜0.01）。A、B、C 3组的踝臂指数（ABI）分别为0.70±0.12、0.58±0.13和1.15±0.07。A、B组ABI均明显低于C组（t=14.749，P＜0.01；t=17.392，P＜0.01），B组ABI明显低于A组（t=3.027， P＜0.05）。SOD与HbA1c呈负相关（r=-0.541，P＜0.01）。A、B两组组内静脉血与动脉血SOD比较差异无统计学意义。B1组、B2组介入前动脉血中SOD水平分别为（35.70±3.04）u/ml，（36.07±2.14）u/ml，二者差异无统计学意义；介入前缺血部位动脉血中SOD水平分别为（32.95±3.52）u/ml，（33.59±2.64）u/ml，二者差异无统计学意义，但均较介入前动脉血中SOD水平明显降低（t=2.741，P＜0.05；t=2.704，P＜0.05）；介入后缺血部位动脉血中SOD水平分别为（29.40±5.49）u/ml，（26.68±2.31）u/ml，二者差异无统计学意义，但均较介入前缺血部位动脉血中的SOD 水平明显降低（t =2.536，P ＜0.05；t =5.005，P ＜0.01）。各部位血中SOD水平B1组B2组间比较差异均无统计学意义。结论静脉血与动脉血中的SOD水平无明显差别；血清中的SOD水平与HbA1c成线性负相关关系；介入术前缺血部位SOD降低，介入术后SOD进一步降低，可能与介入治疗对血管壁损伤导致氧化应激反应增强有关，可能是引起术后再狭窄的危险因素之一。%Objective To observe the changes of serum superoxide dismutase (SOD) levels in typeⅡdiabetic patients with peripheral arterial disease (PAD) before and after interventional therapy, and to investigate the effects of oxidative stress level and interventional treatment on serum SOD level. Methods During the period from July 2011 to December 2012 at authors’ hospital, a total of 40 patients with type Ⅱ angiography together with balloon dilation and/or stenting was carried out in 24 patients (group B, with Fontaine stage of Ⅱb - Ⅲ). Of the 24 patients in group B, lower limb arterial angiography together with balloon dilation was employed in 16 (group B1) and lower limb arterial angiography together with balloon dilation and stenting was adopted in 8 (group B2). Twenty healthy clinical subjects were used as control group (group C). Before interventional treatment, elbow venous blood samples of patients in group A and B were collected to determine serum lipid, HbA1c and SOD levels. The same tests were also carried out in the subjects of group C. During percutaneous lower extremity arterial intervention , through arterial sheath 3 ml arterial blood specimen was collected in all patients of both group A and B before intervention started. Twenty-four hours after the treatment, venous blood specimen was also collected in all patients to determine serum SOD levels. The results were statistically analyzed. Results Lower limb arterial angiography showed that no obvious arterial stenosis was seen in the patients of group A. The interventional procedures were all successfully completed in all patients of group B. SOD levels of group A, B and C were (46.1 ± 3.13)U/ml, (35.37 ± 3.58)U/ml and (60.50 ± 6.99)U/ml respectively. SOD levels of both group A and B were significantly lower than that of group C (t = 8.420, P < 0.01; t = 14.324, P < 0.01). The level of SOD in group A was significantly higher than that in group B (t = 10.092, P < 0.01). The ankle-brachium indexes (ABI) of group A, B and C were (0.70 ± 0.12), (0.58 ± 0.13) and (1.15 ± 0.07) respectively. ABI of group A and B was significantly lower than that of group C (t = 14.324, P < 0.01; t = 17.392, P < 0.01). ABI of group B was significantly lower than that of group A (t=3.027, P<0.05). SOD level bore a negative correlation with HbA1c level (r=-0.541, P<0.01). In both group A and group B, no significant difference in SOD level existed between the venous blood and arterial blood. The preoperative arterial SOD levels in group B1 and group B2 were (35.70 ± 3.04)U/ml, and (36.07 ± 2.14)U/ml respectively, and the difference between the two groups was not statistically significant. The preoperative SOD levels in the ischemic arterial region in group B1 and group B2 were (32.95 ± 3.52)U/ml and (33.59 ± 2.64)U/ml respectively, and the difference between the two groups was not statistically significant although these levels were significantly lower than the preoperative arterial SOD levels(t=2.741, P<0.05; t=2.704, P<0.05). After the interventional treatment, the SOD levels in the ischemic arterial region in group B1 and group B2 were (29.40 ± 5.49)U/ml and (26.68 ± 2.31)U/ml respectively, and the difference between the two groups was not statistically significant although these levels were significantly lower than the preoperative SOD levels in the ischemic arterial region (t = 2.536, P < 0.05; t = 5.005, P < 0.01). No statistically significant differences in SOD levels at each corresponding site existed between group B1 and group B2. Conclusion No significant difference in SOD level exists between the venous blood and the arterial blood. Serum SOD level carries a negative linear correlation with HbA1c level. Before interventional treatment , the SOD level in ischemic region is low, which becomes lower after the interventional procedure, which may be caused by the enhanced oxidative stress reaction that is resulted from the damage of the vascular wall due to interventional manipulations. The enhanced oxidative stress reaction may play an important role in the occurrence of restenosis.
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