CAJ | 학술논문

目的探讨急性肾盂内压升高与不同程度积水肾氧化损伤的关系.方法采用腰大肌包埋法分别建立新西兰大白兔轻度和重度肾积水模型,轻度积水组分为M0、M1、M2和M3组,重度积水组分为S0、S1、S2和S3组,每组6只.对应分别以0、20、60、100 mmHg(1 mmHg =0.133 kPa)压力进行灌注,48 h后取标本分别检测组织中超氧化物歧化酶(SOD)和丙二醛(MDA)含量,并检测组织细胞凋亡.结果轻度积水组经100 mmHg灌注后(M3),组织中SOD和MDA含量分别为(256.9±12.2) U/mg和(0.75±0.03) nmol/mg,细胞凋亡指数为0.66±0.07,和对照组(M0)比较差异有统计学意义(P＜0.05),但M1和M2组变化不明显(P＞0.05);与对照组(S0)比较,重度积水组经60、100 mmHg灌注后(S2和S3),SOD含量分别为(142.0±13.4) U/mg和(138.3±10.2)U/mg,MDA含量分别为(1.01 ±0.01)nmol/mg和(1.03±0.03) nmol/mg,细胞凋亡指数分别为0.64±0.10和0.70±0.07,差异有统计学意义(P＜0.05),但S1与S0比较差异无统计学意义(P＞0.05).结论肾盂灌注压力的升高会引起积水肾的氧化损伤,不同程度积水肾对肾盂灌注压力升高的耐受存在差异.
목적 탐토급성신우내압승고여불동정도적수신양화손상적관계.방법 채용요대기포매법분별건립신서란대백토경도화중도신적수모형,경도적수조분위M0、M1、M2화M3조,중도적수조분위S0、S1、S2화S3조,매조6지.대응분별이0、20、60、100 mmHg(1 mmHg =0.133 kPa)압력진행관주,48 h후취표본분별검측조직중초양화물기화매(SOD)화병이철(MDA)함량,병검측조직세포조망.결과 경도적수조경100 mmHg관주후(M3),조직중SOD화MDA함량분별위(256.9±12.2) U/mg화(0.75±0.03) nmol/mg,세포조망지수위0.66±0.07,화대조조(M0)비교차이유통계학의의(P＜0.05),단M1화M2조변화불명현(P＞0.05);여대조조(S0)비교,중도적수조경60、100 mmHg관주후(S2화S3),SOD함량분별위(142.0±13.4) U/mg화(138.3±10.2)U/mg,MDA함량분별위(1.01 ±0.01)nmol/mg화(1.03±0.03) nmol/mg,세포조망지수분별위0.64±0.10화0.70±0.07,차이유통계학의의(P＜0.05),단S1여S0비교차이무통계학의의(P＞0.05).결론 신우관주압력적승고회인기적수신적양화손상,불동정도적수신대신우관주압력승고적내수존재차이.
Objective To explore the relationship between acute renal pelvis hypertension and oxidative damage in varying degrees of hydronephrosis.Methods The mild and severe hydronephrosis models in New Zealand white rabbits were established by psoas embedding.Mild hydronephrosis group was divided into M0,M1,M2 and M3 subgroups,and severe hydronephrosis group into S0,S1,S2 and S3 subgroups (n =6 each),corresponding to 0,20,60 and 100 mmHg (1 mmHg =0.133 kPa) renal pelvis perfusion pressure,respectively.Specimens were detected after 48 h,including the tissue superoxide dismutase (SOD) and malondialdehyde (MDA) content,and the tissue apoptosis.Results In M3 subgroup,SOD and MDA contents were (256.9 ± 12.2) U/mg and (0.75 ±0.03) nmol/mg,and apoptotic index was 0.66 ± 0.07,which were significantly different from those in M0 subgroup (P ＜ 0.05),but no significant changes were found in M1 and M2 subgroups (P ＞ 0.05).As compared with S0 subgroup,SOD levels were (142.0 ± 13.4) U/mg and (138.3 ± 10.2) U/mg,MDA levels were (1.01 ±0.01) nmol/mg and (1.03 ±0.03) nmol/mg,apoptosis index was 0.64 ±0.10 and 0.70 ±0.07 in S2 and S3 subgroups respectively,which were significantly different from those in S0 subgroup (P ＜ 0.05),but there was no significant difference between S1 subgroup and S0 subgroup.Conclusion Pelvis perfusion pressure rise will cause oxidative damage in hydronephrosis.The tolerance was different in varying degrees of hydronephrosis when the renal pelvis perfusion pressure increased.