Chang Yizhong, Qi Xiaolong, Li Zhiwei, Wang Fei, Wang Shenglan, Zhang Zhaojie, Xiao Chaohui, Ding Tongling, Yang Changqing
Division of Gastroenterology and Hepatology, Tongji Hospital, Tongji University School of Medicine Shanghai 200065, China.
Int J Clin Exp Pathol. 2013 Oct 15;6(11):2523-8. eCollection 2013.
Hepatorenal syndrome is one of the serious complications of cirrhosis and closely associated with the increasing intra-abdominal pressure (IAP). The study aims to explore the potential mechanism of intra-abdominal hypertension in the development of hepatorenal syndrome in mouse models.
Eighty male mice were randomly divided into model group (subcutaneous injection of carbon tetrachloride) and control group (subcutaneous injection of olive oil). After 12 weeks, parts of the mice were sacrificed and liver histopathology was detected. Then, albumin (30 g/L) and normal saline were separately injected into the peritoneal cavity of mice to induce the different IAP levels (0, 5, 10 and 20cmH2O). Blood urea nitrogen, serum creatinine and renal histopathology were examined 24 hours later.
Blood urea nitrogen and serum creatinine levels were statistically significant high in the group of IAP= 10 and 20cmH2O as compared with the IAP= 0cmH2O. From results of renal histopathology, the constrictive renal tubular lumen and inflammatory infiltration in the interstitial were observed in groups of IAP= 5 and 10cmH2O. Besides, the formed casts and hyperemia in the renal interstitial could be detected in group of IAP= 20cmH2O. The cellular swelling and edema of renal tubular epithelial cells were found in model group simultaneously.
Our study suggested that intra-abdominal hypertension was a significant pathological mechanism and a potential independent risk factor of hepatorenal syndrome.
肝肾综合征是肝硬化的严重并发症之一，与腹腔内压力（IAP）升高密切相关。本研究旨在探讨小鼠模型中腹腔内高压在肝肾综合征发生发展中的潜在机制。
80只雄性小鼠随机分为模型组（皮下注射四氯化碳）和对照组（皮下注射橄榄油）。12周后，处死部分小鼠并检测肝脏组织病理学。然后，分别向小鼠腹腔内注射白蛋白（30 g/L）和生理盐水，以诱导不同的IAP水平（0、5、10和20cmH2O）。24小时后检测血尿素氮、血清肌酐和肾脏组织病理学。
与IAP = 0cmH2O组相比，IAP = 10和20cmH2O组的血尿素氮和血清肌酐水平在统计学上显著升高。从肾脏组织病理学结果来看，IAP = 5和10cmH2O组观察到肾小管管腔狭窄和间质炎症浸润。此外，IAP = 20cmH2O组可检测到肾间质中形成的管型和充血。模型组同时发现肾小管上皮细胞肿胀和水肿。
我们的研究表明，腹腔内高压是肝肾综合征的重要病理机制和潜在的独立危险因素。
