摘要
目的观察造影剂所致大鼠急性肾损伤的远期影响。方法 48只雄性SD大鼠经静脉注射消炎痛(10 mg/kg)和L-NG-硝基精氨酸甲酯(L-NAME 10 mg/kg)预处理,30 min后实验组大鼠(n=24)静脉注入复方泛影葡胺(DTZ 8 mL/kg)建立大鼠造影剂所致的急性肾损伤模型,对照组大鼠(n=24)缓慢推注生理盐水8 mL/kg。给药后24 h、1、2、3个月观察大鼠肾功能、肾组织病理学变化。结果对照组和实验组血肌酐基线值无明显差异。实验组注射DTZ 24 h后,血肌酐与基线值相比明显升高[(48.02±5.53)μmol/Lvs.(112.7±45.35)μmol/L,P<0.001],肾组织病理改变以片状小管坏死和间质充血为主,尤以外髓明显;注射DTZ 3个月后,尽管血肌酐与基线值及对照组相比差异无显著统计学意义,但实验组仍存在明显的肾间质局灶性炎症细胞浸润,部分早期损害严重的小管被纤维组织所取代。结论造影剂对大鼠肾脏造成的急性肾损伤并未完全恢复,而留下长期的慢性肾小管间质损伤。
Objective To investigate the long-term effects of contrast medium on renal function in a rat contrast-induced nephropathy(CIN) modle. Methods Forty-eight SD rats were pretreated intravenously with L-NG-nitroarginine methyl ester(L-NAME 10 mg/kg) and indomethacin(10 mg/kg).Then 30 minutes later diatrizoate(DTZ 8 mL/kg) was administrated in test group(n=24) to establish contrast-induced acute renal injury models,and saline(8 mL/kg) was injectd in control group(n=24).Renal function and histopathological changes were monitored at 24 hours,and at the end of 1st,2nd and 3rd month after the administration. Results There was no significant difference of serum creatinine baseline value between test and control group.Twenty-four hours after DTZ injection,serum creatinine in test group increased significantly from(48.02±5.53)μmol/L to(112.7±45.35)μmol/L(P0.001).Meanwhile,the pathological changes were characterized by extensive cytoplasmic disruption,interstitial congestion and edema,especially in the outer medulla.Although serum creatinine dropped back to the baseline 3 months after DTZ injection in test group,focal interstitial inflamation still existed,and rave lesions of the tubulointerstitium were partly replaced by fibrous tissues. Conclusions Renal function of the SD rats may not recover completely 3 months after DTZ administration as the maintenance of chronic tubulointerstitial lesions.
出处
《复旦学报(医学版)》
CAS
CSCD
北大核心
2011年第1期18-21,共4页
Fudan University Journal of Medical Sciences
基金
复旦大学青年科学基金项目(2007-217)
关键词
造影剂
急性肾损伤
慢性肾小管间质损伤
大鼠
contrast media
acute renal injury
chronic renal tubulointerstitial injury
rats