CAJ | 학술논문

目的：研究急性脑出血对肠粘膜屏障功能的影响。方法：成年雄性Wistar大鼠60只，随机分为脑出血组和对照组各30只。脑出血组采用立体定向技术将大鼠自体尾动脉不抗凝动脉血液50μL缓慢注入尾状核制备脑出血模型，对照组注射等量生理盐水。2组分别于造模前和造模后0.5、3、6、12、24 h检测血浆二胺氧化酶（DAO）活性和D-乳酸（D-Lac）浓度，于造模前和造模后12、24 h检测血浆内毒素（LPS）浓度；造模后24 h取空肠l cm，光镜下观察肠粘膜。结果：与对照组比较，脑出血组造模后12、24 h DAO活性和造模后6、12、24 h D-Lac浓度及造模后12、24 h LPS浓度明显增高，差异有统计学意义（＜0.05或＜0.01）。光镜下观察，脑出血组小肠存在病理性损伤，对照组小肠结构正常。结论：急性脑出血早期即发生肠屏障功能障碍。
목적：연구급성뇌출혈대장점막병장공능적영향。방법：성년웅성Wistar대서60지，수궤분위뇌출혈조화대조조각30지。뇌출혈조채용입체정향기술장대서자체미동맥불항응동맥혈액50μL완만주입미상핵제비뇌출혈모형，대조조주사등량생리염수。2조분별우조모전화조모후0.5、3、6、12、24 h검측혈장이알양화매（DAO）활성화D-유산（D-Lac）농도，우조모전화조모후12、24 h검측혈장내독소（LPS）농도；조모후24 h취공장l cm，광경하관찰장점막。결과：여대조조비교，뇌출혈조조모후12、24 h DAO활성화조모후6、12、24 h D-Lac농도급조모후12、24 h LPS농도명현증고，차이유통계학의의（＜0.05혹＜0.01）。광경하관찰，뇌출혈조소장존재병이성손상，대조조소장결구정상。결론：급성뇌출혈조기즉발생장병장공능장애。
ObjectiveTo observe the changes of intestinal barrier function of rats with acute cerebral hemorrhage. Methods:Sixty Wistar rats were randomly divided into cerebral hemorrhage group and control group with 30 rats in each group. The cerebral hemorrhage model was established by stereotactic infusing 50 μL autologous caudate artery blood. The control group were only infused with equal normal saline. The concentra-tion of plasma diamine oxidase (DAO) and activity of D-lactate (D-lac) in plasma were measured before operation and 0.5, 3, 6, 12, 24 h after operation. The concentration of plasma Lipopolysaccharide (LPS) was measured before operation and 12, 24 h after operation. The jejunums (1 cm) of the both groups were taken at 24 h after operation, and light microscopic examination was performed for morphological measurement of intestinal epithelial cells. Results:Compared with those in the control group, the DAO and LPS concentrations at 12, 24 h and the D-lac levels at 6,12, 24 h after operation were significantly increased in the cerebral hemorrhage group ( <0.05 or 0.01). Under the light microscope, intestinal mucosal injuries were observed in the cerebral hemorrhage group whereas no obvious changes occurred in the control group . Conclusion:Intestinal barrier function was damaged in the early stage of cerebral hemorrhage.