介入放射学杂志
介入放射學雜誌
개입방사학잡지
JOURNAL OF INTERVENTIONAL RADIOLOGY
2014年
9期
762-766
,共5页
侯琳%王富军%李艳艳%齐会卿%张玉娜%白磊%孙金
侯琳%王富軍%李豔豔%齊會卿%張玉娜%白磊%孫金
후림%왕부군%리염염%제회경%장옥나%백뢰%손금
糖尿病%下肢血管病变%介入治疗%超氧化物歧化酶(SOD)
糖尿病%下肢血管病變%介入治療%超氧化物歧化酶(SOD)
당뇨병%하지혈관병변%개입치료%초양화물기화매(SOD)
diabetes mellitus%vascular disease of lower extremity%interventional treatment%superoxide dismutase
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。
目的：觀察2型糖尿病（T2DM）下肢血管病變（PAD）患者下肢動脈介入治療前後病變動脈血清中超氧化物歧化酶（SOD）水平的變化，探討T2DM閤併PAD患者體內氧化應激水平及介入治療對血清SOD的影響。方法選擇2011年7月-2012年12月接受介入治療的T2DM閤併PAD患者40例，其中下肢單純動脈造影者（A組）16例，行下肢動脈造影、毬囊擴張及支架植入者（B組）24例（Fontaine分期Ⅱb期和Ⅲ期的患者）。B組中，單純行下肢動脈造影、毬囊擴張者16例（B1組），行下肢動脈造影、毬囊擴張且行支架植入者8例（B2組）。門診健康體檢者（C組）20名作為對照組。A、B兩組介入術前行常規檢查併取靜脈血測血脂、糖化血紅蛋白（HbA1c）和SOD水平。 C組在同樣條件下抽取肘靜脈血測定上述指標。A、B兩組術中取介入前動脈血，術後24 h取靜脈血測定各組血清SOD水平。結果 A組患者下肢動脈造影無明顯狹窄。 A、B、C 3組SOD分彆為（46.1±3.13）u/ml，（35.37±3.58）u/ml，（60.50±6.99）u/ml， A、B組SOD水平均明顯低于C組（t=8.420，P＜0.01；t=14.324，P＜0.01），A組SOD水平明顯高于B組（t=10.092，P＜0.01）。A、B、C 3組的踝臂指數（ABI）分彆為0.70±0.12、0.58±0.13和1.15±0.07。A、B組ABI均明顯低于C組（t=14.749，P＜0.01；t=17.392，P＜0.01），B組ABI明顯低于A組（t=3.027， P＜0.05）。SOD與HbA1c呈負相關（r=-0.541，P＜0.01）。A、B兩組組內靜脈血與動脈血SOD比較差異無統計學意義。B1組、B2組介入前動脈血中SOD水平分彆為（35.70±3.04）u/ml，（36.07±2.14）u/ml，二者差異無統計學意義；介入前缺血部位動脈血中SOD水平分彆為（32.95±3.52）u/ml，（33.59±2.64）u/ml，二者差異無統計學意義，但均較介入前動脈血中SOD水平明顯降低（t=2.741，P＜0.05；t=2.704，P＜0.05）；介入後缺血部位動脈血中SOD水平分彆為（29.40±5.49）u/ml，（26.68±2.31）u/ml，二者差異無統計學意義，但均較介入前缺血部位動脈血中的SOD 水平明顯降低（t =2.536，P ＜0.05；t =5.005，P ＜0.01）。各部位血中SOD水平B1組B2組間比較差異均無統計學意義。結論靜脈血與動脈血中的SOD水平無明顯差彆；血清中的SOD水平與HbA1c成線性負相關關繫；介入術前缺血部位SOD降低，介入術後SOD進一步降低，可能與介入治療對血管壁損傷導緻氧化應激反應增彊有關，可能是引起術後再狹窄的危險因素之一。
목적：관찰2형당뇨병（T2DM）하지혈관병변（PAD）환자하지동맥개입치료전후병변동맥혈청중초양화물기화매（SOD）수평적변화，탐토T2DM합병PAD환자체내양화응격수평급개입치료대혈청SOD적영향。방법선택2011년7월-2012년12월접수개입치료적T2DM합병PAD환자40례，기중하지단순동맥조영자（A조）16례，행하지동맥조영、구낭확장급지가식입자（B조）24례（Fontaine분기Ⅱb기화Ⅲ기적환자）。B조중，단순행하지동맥조영、구낭확장자16례（B1조），행하지동맥조영、구낭확장차행지가식입자8례（B2조）。문진건강체검자（C조）20명작위대조조。A、B량조개입술전행상규검사병취정맥혈측혈지、당화혈홍단백（HbA1c）화SOD수평。 C조재동양조건하추취주정맥혈측정상술지표。A、B량조술중취개입전동맥혈，술후24 h취정맥혈측정각조혈청SOD수평。결과 A조환자하지동맥조영무명현협착。 A、B、C 3조SOD분별위（46.1±3.13）u/ml，（35.37±3.58）u/ml，（60.50±6.99）u/ml， A、B조SOD수평균명현저우C조（t=8.420，P＜0.01；t=14.324，P＜0.01），A조SOD수평명현고우B조（t=10.092，P＜0.01）。A、B、C 3조적과비지수（ABI）분별위0.70±0.12、0.58±0.13화1.15±0.07。A、B조ABI균명현저우C조（t=14.749，P＜0.01；t=17.392，P＜0.01），B조ABI명현저우A조（t=3.027， P＜0.05）。SOD여HbA1c정부상관（r=-0.541，P＜0.01）。A、B량조조내정맥혈여동맥혈SOD비교차이무통계학의의。B1조、B2조개입전동맥혈중SOD수평분별위（35.70±3.04）u/ml，（36.07±2.14）u/ml，이자차이무통계학의의；개입전결혈부위동맥혈중SOD수평분별위（32.95±3.52）u/ml，（33.59±2.64）u/ml，이자차이무통계학의의，단균교개입전동맥혈중SOD수평명현강저（t=2.741，P＜0.05；t=2.704，P＜0.05）；개입후결혈부위동맥혈중SOD수평분별위（29.40±5.49）u/ml，（26.68±2.31）u/ml，이자차이무통계학의의，단균교개입전결혈부위동맥혈중적SOD 수평명현강저（t =2.536，P ＜0.05；t =5.005，P ＜0.01）。각부위혈중SOD수평B1조B2조간비교차이균무통계학의의。결론정맥혈여동맥혈중적SOD수평무명현차별；혈청중적SOD수평여HbA1c성선성부상관관계；개입술전결혈부위SOD강저，개입술후SOD진일보강저，가능여개입치료대혈관벽손상도치양화응격반응증강유관，가능시인기술후재협착적위험인소지일。
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.
