摘要
目的研究地塞米松对蛛网膜下腔出血(SAH)后交通性脑积水的防治作用,并探讨蛛网膜下腔出血后交通性脑积水的形成机制。方法用自体左心室血通过枕大池注入蛛网膜下腔制做蛛网膜下腔出血模型,实验设为一个对照组和一个实验组,每组16只大鼠,对照组在蛛网膜下腔内注一定量的自体血,实验组注射一定量的自体血和药物,按模型完成后第1天和第20天各组再均分为两组,观察各组到预期时间点时脑脊液TGF-β1浓度和软脑膜胶原纤维厚度。脑脊液TGF-β1浓度通过ELISA法检测,脑组织用Massion’s三重染色法染色后用图像分析系统测软脑膜厚度。结果实验组SAH后期脑脊液TGF-β1过度表达和软脑膜胶原纤维增生厚均低于对照组(P〈0.01)。且二者成正相关。结论地塞米松可以抑制SAH后期脑脊液TGF-β1过度表达及后期软脑膜胶原纤维增生,为临床地塞米松防治蛛网膜下腔出血后交通性脑积水提供了实验和理论依据。
Objective To study the preventive and therapeutic effect of dexamethasone on commu- nicating hydrocephalus following subarachnoid hemorrhage (SAH) , and explore the mechanism of communicating hydrocephalus following SAH. Methods SAH rat model was constructed by injecting auto blood through foramen magnum into subarachnoid space. There were two groups (one control group and one experimental group) in this study with 16 rats each group. Sufficient doses of auto blood were injected into subarachnoid space of the rats of the control group and sufficient dose of auto blood together with sufficient dose of dexamethasone into subarachnoid space of the rats of the experimental group. The changes of rat's transforming growth factor bata-1 (TGF-β1)in the cerebrospinal fluid (CSF)and thickness of pia mater collagen fibrosis(CF) following SAH were observed after 1 clay and 20 days. The levels of TGF-β1 in the CSF were quantitatively detected by the way of ABC-ELISA. The brain tissues were clyed through Massion's technique, and then the average thicknesses of meningina CF were measured by the software of mierograph collection and analysis computer system. Results In later stage after SAH, TGF-β1 concentrations of the experimental group was lower than control group( P 〈 0. 01 ). At the same time, the average thicknesses of meningina CF of experimental groups was thinner than control group( P 〈0. 01 ). Moreover, the relationship between the level of TGF-β1 in the CSF and the thickness of the CF of the rat's cerebral pia mate had positive correlation. Conclusions In the later stage after SAH, dexamethasone can inhibit the over expression of TGF-β1 in rat CSF following SAH and also can inhibit the accrementition of rat collagenous fibers. Therefore, this study provided experimental and theoretical evidence for preventing and treating communicating hydrocephalus following SAH.
出处
《中国医师杂志》
CAS
2010年第1期59-62,共4页
Journal of Chinese Physician