中华创伤杂志
中華創傷雜誌
중화창상잡지
Chinese Journal of Traumatology
2008年
7期
502-505
,共4页
杨树旭%信照亮%钱聪%王义荣
楊樹旭%信照亮%錢聰%王義榮
양수욱%신조량%전총%왕의영
蛛网膜下腔出血%纤维变性%地塞米松
蛛網膜下腔齣血%纖維變性%地塞米鬆
주망막하강출혈%섬유변성%지새미송
Subarachnoid hemorrhage%Fibrosis%Dexamethasone
目的 探讨蛛网膜下腔出血(subarachnoid hemorrhage,SAH)后蛛网膜纤维化的发生机制.方法 实验大鼠分成对照组、实验组、治疗组,使用放射免疫法(RIA)测定蛛网膜中透明质酸(HA)、层黏连蛋白(LN)、Ⅲ型前胶原氨基端肽(PⅢNP)、Ⅳ型胶原的含量.应用电镜观察蛛网膜细胞的形态及蛛网膜胶原纤维分布情况.结果 RIA 测量的4种细胞外基质中,PⅢNP在出血后增高最明显,LN与HA也明显升高,而Ⅳ型胶原变化不明显.应用地塞米松治疗后PmNP明显降低.电镜下发现蛛网膜细胞在出血后其生物活性增强,蛛网膜下腔的胶原纤维在1周左右开始明显增多,持续3周以上,地塞米松治疗后蛛网膜细胞线粒体密度相对较低,蛛网膜胶原纤维较稀疏.结论 蛛网膜下腔出血后细胞外基质明显增加,参与蛛网膜纤维化.地塞米松可减轻蛛网膜下腔出血后蛛网膜纤维化,为防治蛛网膜下腔出血后脑积水提供新的思路.
目的 探討蛛網膜下腔齣血(subarachnoid hemorrhage,SAH)後蛛網膜纖維化的髮生機製.方法 實驗大鼠分成對照組、實驗組、治療組,使用放射免疫法(RIA)測定蛛網膜中透明質痠(HA)、層黏連蛋白(LN)、Ⅲ型前膠原氨基耑肽(PⅢNP)、Ⅳ型膠原的含量.應用電鏡觀察蛛網膜細胞的形態及蛛網膜膠原纖維分佈情況.結果 RIA 測量的4種細胞外基質中,PⅢNP在齣血後增高最明顯,LN與HA也明顯升高,而Ⅳ型膠原變化不明顯.應用地塞米鬆治療後PmNP明顯降低.電鏡下髮現蛛網膜細胞在齣血後其生物活性增彊,蛛網膜下腔的膠原纖維在1週左右開始明顯增多,持續3週以上,地塞米鬆治療後蛛網膜細胞線粒體密度相對較低,蛛網膜膠原纖維較稀疏.結論 蛛網膜下腔齣血後細胞外基質明顯增加,參與蛛網膜纖維化.地塞米鬆可減輕蛛網膜下腔齣血後蛛網膜纖維化,為防治蛛網膜下腔齣血後腦積水提供新的思路.
목적 탐토주망막하강출혈(subarachnoid hemorrhage,SAH)후주망막섬유화적발생궤제.방법 실험대서분성대조조、실험조、치료조,사용방사면역법(RIA)측정주망막중투명질산(HA)、층점련단백(LN)、Ⅲ형전효원안기단태(PⅢNP)、Ⅳ형효원적함량.응용전경관찰주망막세포적형태급주망막효원섬유분포정황.결과 RIA 측량적4충세포외기질중,PⅢNP재출혈후증고최명현,LN여HA야명현승고,이Ⅳ형효원변화불명현.응용지새미송치료후PmNP명현강저.전경하발현주망막세포재출혈후기생물활성증강,주망막하강적효원섬유재1주좌우개시명현증다,지속3주이상,지새미송치료후주망막세포선립체밀도상대교저,주망막효원섬유교희소.결론 주망막하강출혈후세포외기질명현증가,삼여주망막섬유화.지새미송가감경주망막하강출혈후주망막섬유화,위방치주망막하강출혈후뇌적수제공신적사로.
Objective To study the mechanism of arachnoidal fibrosis after subarachnoid hemor- rhage. Methods Rats were divided into control group, experiment group and treatment group. Radioim- munoassay (RIA) was employed to detect the levels of hyaluronic acid, laminin,type Ⅲ precollagen and type Ⅳ collagen in the arachnoid membrane. In the meantime, arachnoid cell's morphology and collagen distribution in the subarachnoid space were investigated by electron microscope. Results Results of RIA detection showed increase of Type Ⅲ precollagen level (peak at the second week), obvious higher levels of LN and HA but insignificant change of type IV collagen after subarachnoid hemorrhage. However, dexam- ethasone treatment decreased type Ⅲ precollagen level. Electron microscope found that arachnoid cells pres- ented accentruated bioactivity after subarachnoid hemorrhage, with significant increase of arachnoidal colla- gen fibers from one week after suharachnoid hemorrhage, continuing for 3 weeks. Dexamethasone treatment resulted in low density of mitochondria and sparsed arachnoidal collagen fibers. Conclusions Extracellu- lar matrix (ECM) increases in arachnoid membrane after subarachnoid hemorrhage and participates in a- rachnoid fibrosis. Dexamethasoue can relieve arachnoidal fibrosis after subarachnoid hemorrhage, as pro- rides fresh way for prevention and treatment of post hemorrhagic hydrocephalus.