Establishment of a rat model ofalcohol-induced avascular necrosis of the femoral head
10.3969/j.issn.2095-4344.2016.27.004
- VernacularTitle:酒精性股骨头缺血坏死大鼠模型的制备
- Author:
Yun YANG
;
Haiyan FAN
;
Jian HUANG
;
Zhongping MA
;
Zhifeng ZHANG
- Publication Type:Journal Article
- From:
Chinese Journal of Tissue Engineering Research
2016;20(27):3977-3983
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND:The relationship between long-term heavy drinking and alcohol-induced necrosis of the femoral head has long been clear, but thepathogenesis of alcohol-induced necrosis of the femoral head is currently not fuly understood.
OBJECTIVE:To establish a rat model of alcohol-induced avascular necrosis of femoral head and to study its pathogenesis.
METHODS: Eighty Wistar rats were randomly divided into experimental and control groups (40 rats per group). Rats in the experimental group were intragastricaly administered strong wine 10 mL/kg, once a day, for 6 consecutive days. Rats in the control group were given physiological saline 10mL/kg, once a day, for 6 consecutive days. Bilateral femoral heads were randomly colected from six rats every month for histomorphological observation.
RESULTS AND CONCLUSION:(1) Osteonecrosis: in the experimental group, at 3 months, trabecular bone became thin, arranged disorderly, and the number of empty lacuna began to increase. At 6 months, typical osteonecrosis appeared, and vacant lacunaes increased significantly. In the control group, trabecular bone was complete and neatly arranged. Osteocytes were visible in bone lacuna, and normal morphology of cels was seen. (2) Injury of blood vessels: in the experimental group, at 3 months, micro-intimal hyperplasia was observed. Elastic fibers of partial vascular endothelium were reduced. Elastic fiber andmiddle-layer smooth muscle breakage and proliferation were found. At 6 months, above manifestations were more remarkable. In the control group, arteriole film was not thickened, and vessel wal was normal. (3) Formation of microthrombus, in the experimental group, the number of microthrombus was increased at 3 months, and became significant at 6 months. In the control group, the number of microthrombus was not altered. (4) Results indicated that chronic alcohol intake can lead to microvascular endothelial injury in the rat femoral head. Abnormal blood microcirculation was detected in local region, and resulted in avascular necrosis of the femoral head. The degree of necrosis was associated with alcohol intake.
