CAJ | 학술논문

目的观察急性肾盂内压升高对不同程度积水肾线粒体损伤的影响.方法采用腰大肌包埋法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,对应分别以0、20、60、100 mmHg(1 mmHg =0.133 kPa)压力进行肾盂灌注,观察肾组织标本线粒体超微结构改变和线粒体膜电位的变化.结果轻度积水组经100 mmHg灌注后(M3),线粒体空泡化比例为(66.33 ±4.42)％,JC-1多聚体/单体荧光强度(Q2/Q4)的值为0.36±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),线粒体空泡化比例分别为(85.67±8.61)％和(87.50±5.77)％,Q2/Q4的值分别为0.42±0.07和0.23±0.04,差异有统计学意义(P＜0.05),但S1与SO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导致线粒体空泡化和膜电位降低,不同程度积水肾对肾盂内压升高的耐受能力存在差异.
목적 관찰급성신우내압승고대불동정도적수신선립체손상적영향.방법 채용요대기포매법건립신서란대백토경도화중도신적수모형,경도적수조분위M0、M1、M2화M3조,중도적수조분위S0、S1、S2화S3조,대응분별이0、20、60、100 mmHg(1 mmHg =0.133 kPa)압력진행신우관주,관찰신조직표본선립체초미결구개변화선립체막전위적변화.결과 경도적수조경100 mmHg관주후(M3),선립체공포화비례위(66.33 ±4.42)％,JC-1다취체/단체형광강도(Q2/Q4)적치위0.36±0.07,화대조조(M0)비교차이유통계학의의(P＜0.05),단M1화M2조변화불명현(P＞0.05);여대조조(S0)비교,중도적수조경60、100 mmHg관주후(S2화S3),선립체공포화비례분별위(85.67±8.61)％화(87.50±5.77)％,Q2/Q4적치분별위0.42±0.07화0.23±0.04,차이유통계학의의(P＜0.05),단S1여SO비교차이무통계학의의(P＞0.05).결론 신우관주압력적승고회도치선립체공포화화막전위강저,불동정도적수신대신우내압승고적내수능력존재차이.
Objective To investigate the mitochondrial damage of acute increased renal pelvis pressure to varying degrees of hydronephrosis.Methods The mild and severe hydronephrosis model in New Zealand white rabbits were established by psoas Embedding.Mild hydronephrosis group was divided into M0,M1,M2 and M3 group,severe hydronephrosis group was divided into S0,S1,S2 and S3 groups (n =6),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 ultrastructural alterations observed and the mitochondrial membrane potential detected.Results The group of 100 mmHg perfusion (M3) in mild hydronephrosis,vacuolization of mitochondria ratio was (66.33 ± 4.42) ％ and the value of JC-1 polymer/ monomer fluorescence intensity (Q2/Q4) was 0.36 ± 0.07,which were significantly alter when compared to control group (M0,P ＜ 0.05),but no significant changes in M1 and M2 group (P ＞ 0.05).Compared with the control group (S0),severe hydronephrosis group by 60 and 100 mmHg perfusion (S2 and S3),vacuolization of mitochondria ratio were (85.67 ± 8.61) ％ and (87.50 ± 5.77) ％,while the Q2/Q4 were 0.42 ± 0.07 and 0.23 ± 0.04,which were significantly changed (P ＜ 0.05),but no significant change in the S1 group.Conclusion Pelvis perfusion pressure rise will cause mitochondrial vacuolization and membrane potential decreases,the tolerance was differences in varying degrees of hydronephrosis when the renal pelvis perfusion pressure increased.