Department of Gerontology, Tianjin Medical University General Hospital, Tianjin, China.
Sleep Breath. 2011 Sep;15(3):493-502. doi: 10.1007/s11325-010-0370-3. Epub 2010 Jun 27.
Sleep apnea-hypopnea syndrome and its chronic intermittent hypoxia component may cause multi-system-targeted injury. The latest finding shows that liver is one of the injured organs. The purpose of the study is to observe the dynamic process of the influence that chronic intermittent hypoxia plays on rat liver enzyme, hepatic histology, and ultrastructure based on lipid disorders.
A total of 72 male Wistar rats were randomly divided into three groups. The control group was fed with a regular chow diet, the high fat group with a high fat diet, and the high fat plus intermittent hypoxia group with a high fat diet with a 7-h/day intermittent hypoxia treatment. Changes were observed in rat liver enzyme, hepatic histology, and ultrastructure of the three groups on the third, sixth, and ninth weeks, respectively. The liver paraffin sections were detected with myeloperoxidase.
The liver function and structure of the control group were found to be normal; the liver enzyme level of the high fat group was significantly higher than that of the control group on the sixth and ninth weeks; and the liver enzyme level of the high fat plus intermittent hypoxia group was significantly higher than that of the control group and the high fat group on the third, sixth, and ninth weeks (all P < 0.01). Observed by a light microscope and a transmission electron microscope, the high fat group and the high fat plus intermittent hypoxia group were all characterized by nonalcoholic fatty liver disease: the high fat group was characterized by simple fatty liver on the third and sixth weeks and by steatohepatitis on the ninth week; the damage of the high fat plus intermittent hypoxia group was significantly more severe than that of the high fat group in all the monitoring points, characterized by steatohepatitis on the sixth week and by obvious liver fibrosis on the ninth week; the myeloperoxidase level of the high fat plus intermittent hypoxia group was significantly higher than that of the control group and the high fat group (all P < 0.01).
Under the conditions of high fat and intermittent hypoxia, the injury to the liver function, hepatic histology, and ultrastructure is more severe than that of the high fat group. The injury mainly was characterized by nonalcoholic fatty liver disease and becomes more severe with increased exposure time. Oxidative stress may play an important role in the mechanism.
睡眠呼吸暂停低通气综合征及其慢性间歇性低氧成分可能导致多系统靶向损伤。最新发现表明,肝脏是受损器官之一。本研究的目的是观察基于脂质紊乱的慢性间歇性低氧对大鼠肝酶、肝组织学和超微结构的影响的动态过程。
将 72 只雄性 Wistar 大鼠随机分为三组。对照组给予常规饲料,高脂组给予高脂饲料,高脂加间歇性低氧组给予高脂饲料加 7 小时/天的间歇性低氧处理。分别于第 3、6、9 周观察三组大鼠肝酶、肝组织学和超微结构的变化。采用髓过氧化物酶检测肝石蜡切片。
对照组肝功能和结构正常;高脂组第 6、9 周肝酶水平明显高于对照组(均 P<0.01);高脂加间歇性低氧组第 3、6、9 周肝酶水平明显高于对照组和高脂组(均 P<0.01)。光镜和透射电镜观察,高脂组和高脂加间歇性低氧组均表现为非酒精性脂肪性肝病:高脂组第 3、6 周表现为单纯性脂肪肝,第 9 周表现为脂肪性肝炎;高脂加间歇性低氧组损伤明显较高脂组严重,各监测点均表现为脂肪性肝炎,第 9 周表现为明显肝纤维化;高脂加间歇性低氧组髓过氧化物酶水平明显高于对照组和高脂组(均 P<0.01)。
在高脂和间歇性低氧条件下,肝酶、肝组织学和超微结构的损伤比高脂组更严重。损伤主要表现为非酒精性脂肪性肝病,随着暴露时间的增加而加重。氧化应激可能在发病机制中起重要作用。