中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2010年
11期
1378-1380
,共3页
刘燕%夏晓红%苗智慧%王燕凌%洪丽华
劉燕%夏曉紅%苗智慧%王燕凌%洪麗華
류연%하효홍%묘지혜%왕연릉%홍려화
硝苯地平%肾%再灌注损伤
硝苯地平%腎%再灌註損傷
초분지평%신%재관주손상
Nifedipine%Kidney%Reperfusion injury
目的 探讨硝苯地平对大鼠肾缺血再灌注损伤的影响.方法 健康雄性SD大鼠42只,体重220~250 g,随机分为3组(n=14):假手术组(S组)、缺血再灌注组(IR组)和硝苯地平组(N组).IR组和N组采用夹闭双侧肾动、静脉45 min后恢复灌注的方法制备大鼠肾缺血再灌注模型,S组不夹闭双侧肾动、静脉.N组于夹闭前15 min和再灌注前15 min分别尾静脉注射硝苯地平0.1 mg/kg,IR组分别尾静脉注射等量溶剂.于再灌注6和24 h时留尿,测定尿N-乙酰-β-D-氨基葡萄糖苷酶(NAG)活性;抽取腹主动脉血,测定血清肌酐(Cr)、MDA和一氧化氮(NO)浓度,然后处死大鼠取肾,采用流式细胞仪检测肾皮质细胞凋亡情况、热休克蛋白70(HSP70)的表达,免疫组化法测定内皮素-1(ET-1)的表达.结果 与S组比较,IR组血清Cr和MDA浓度、尿NAG活性、HSP70和ET-1表达水平及肾皮质细胞凋亡率均升高(P<0.05),血清NO浓度差异无统计学意义(P>0.05);与IR组比较,N组血清Cr和MDA浓度、尿NAG活性、ET-1表达水平及肾皮质细胞凋亡率降低,血清NO浓度升高(P<0.05),HSP70表达水平差异无统计学意义(P>0.05).结论 硝苯地平可减轻大鼠肾缺血再灌注损伤,可能与其抑制ET-1表达有关.
目的 探討硝苯地平對大鼠腎缺血再灌註損傷的影響.方法 健康雄性SD大鼠42隻,體重220~250 g,隨機分為3組(n=14):假手術組(S組)、缺血再灌註組(IR組)和硝苯地平組(N組).IR組和N組採用夾閉雙側腎動、靜脈45 min後恢複灌註的方法製備大鼠腎缺血再灌註模型,S組不夾閉雙側腎動、靜脈.N組于夾閉前15 min和再灌註前15 min分彆尾靜脈註射硝苯地平0.1 mg/kg,IR組分彆尾靜脈註射等量溶劑.于再灌註6和24 h時留尿,測定尿N-乙酰-β-D-氨基葡萄糖苷酶(NAG)活性;抽取腹主動脈血,測定血清肌酐(Cr)、MDA和一氧化氮(NO)濃度,然後處死大鼠取腎,採用流式細胞儀檢測腎皮質細胞凋亡情況、熱休剋蛋白70(HSP70)的錶達,免疫組化法測定內皮素-1(ET-1)的錶達.結果 與S組比較,IR組血清Cr和MDA濃度、尿NAG活性、HSP70和ET-1錶達水平及腎皮質細胞凋亡率均升高(P<0.05),血清NO濃度差異無統計學意義(P>0.05);與IR組比較,N組血清Cr和MDA濃度、尿NAG活性、ET-1錶達水平及腎皮質細胞凋亡率降低,血清NO濃度升高(P<0.05),HSP70錶達水平差異無統計學意義(P>0.05).結論 硝苯地平可減輕大鼠腎缺血再灌註損傷,可能與其抑製ET-1錶達有關.
목적 탐토초분지평대대서신결혈재관주손상적영향.방법 건강웅성SD대서42지,체중220~250 g,수궤분위3조(n=14):가수술조(S조)、결혈재관주조(IR조)화초분지평조(N조).IR조화N조채용협폐쌍측신동、정맥45 min후회복관주적방법제비대서신결혈재관주모형,S조불협폐쌍측신동、정맥.N조우협폐전15 min화재관주전15 min분별미정맥주사초분지평0.1 mg/kg,IR조분별미정맥주사등량용제.우재관주6화24 h시류뇨,측정뇨N-을선-β-D-안기포도당감매(NAG)활성;추취복주동맥혈,측정혈청기항(Cr)、MDA화일양화담(NO)농도,연후처사대서취신,채용류식세포의검측신피질세포조망정황、열휴극단백70(HSP70)적표체,면역조화법측정내피소-1(ET-1)적표체.결과 여S조비교,IR조혈청Cr화MDA농도、뇨NAG활성、HSP70화ET-1표체수평급신피질세포조망솔균승고(P<0.05),혈청NO농도차이무통계학의의(P>0.05);여IR조비교,N조혈청Cr화MDA농도、뇨NAG활성、ET-1표체수평급신피질세포조망솔강저,혈청NO농도승고(P<0.05),HSP70표체수평차이무통계학의의(P>0.05).결론 초분지평가감경대서신결혈재관주손상,가능여기억제ET-1표체유관.
Objective To investigate the effect of nifedipine on renal ischemia-reperfusion injury (I/R) in rats and the possible mechanism. Methods Forty-two male SD rats weighing 220-250 g were randomly divided into 3 groups with 14 animals in each group: sham operation group (group S); I/R group and I/R + nifedipine group (group N). The renal ischemia was induced by occlusion of bilateral renal arteries and veins for 45 min followed by reperfusion. In group S the renal arteries and veins were only exposed but not occluded. In group N, nifedipine 0.1 mg/kg was injected via the tail vein 15 min before ischemia and 15 min before reperfusion, while the equal volume of solvent was given in group I/R. The urine was collected to detect the N-acetyl-β-D-glucosaminide (NAG) activities at 6 and 24 h of reperfusion. Arterial blood samples were taken at 6 and 24 h reperfusion for determination of concentrations of serum creatinine (Cr), malondialdehyde (MDA) and NO. The rats were then sacrificed and the kidney was removed to detect the apoptotic cells in renal cortex and expression of heat shock protein 70 (HSP70) and endothelin- 1 (ET-1). Results The concentrations of serum Cr and MDA, NAG activity, expression of HSP70 and ET-1 and apoptosis rate were significantly increased in group I/R compared with group S (P <0.05). The concentrations of serum Cr and MDA, NAG activity, ET-1 expression and apoptosis rate were significantly decreased, while the serum NO concentration was significantly increased in group N compared with group I/R (P < 0.05). Conclusion Nifedipine can attenuate renal I/R injury and the underlying mechanism may be related to the inhibition of ET-1 expression.