Permanent focal cerebral ischemia and global ischemia models have been established in our laboratory recently . also , we have found that ono - 1078 , a selective cysteinyl - leukotriene receptor antagonist , is protective against ischemic brain injury due to the permanent focal cerebral ischemia 本实验室在脑缺血损伤研究中，已建立了整体局灶性脑缺血(大脑中动脉阻塞， mcao )和全脑缺血(四血管阻断， 4vo )模型。
Objective to report 16 cases of intracranial aneurysms with calcified vascular wall and study the relationship between vascular calcification and pathogenic mechanism of intracranial aneurysms . methods spiral ct scan , clinical data and serum calcium , phosphate , glucose , lipid , renal function of the 16 patients were studied in retrospect . all aneurysms were clipped , in which 8 were resected after clipping . results the location of aneurysms with aneurismal wall calcification was , on posterior communicating artery in 3 , on middle cerebral artery in 2 , on anterior communicating artery in 2 , on basilar artery in 5 and on basilar artery in 4 . all patients showed normal serum calcium , phosphate , glucose and normal renal function . serum lipid of patients had been elevated . all patients recovered with no significant neurological deficits . conclusion intracranial vascular calcification is an active and regulated process in close relation to atherosclerosis , serum calcium , phosphate , lipid , thyroid , parathyroid function and other factors . intracranial vascular calcification has close relationship with the pathogenesis and management of intracranial aneurysms 目的报告16例瘤壁有钙化的颅内动脉瘤病例的治疗,分析颅内血管钙化与颅内动脉瘤病理发生机制的关系.方法回顾性分析16例瘤壁有钙化的颅内动脉瘤病例的影像学、临床资料及手术治疗.结果瘤壁有钙化的颅内动脉瘤的位置是: 3例位于后交通动脉, 2例位于大脑中动脉, 2例位于前交通动脉, 5例位于椎动脉, 4例位于基底动脉.所有患者血钙、磷酸盐、血糖、肾功能正常. 6例患者血脂增高. 16例患者均行动脉瘤夹闭术,其中8例术中切除动脉瘤,治疗效果良好.结论动脉瘤瘤壁钙化与其病理发生机制有关,常见于巨大或大动脉瘤,瘤壁血管钙化是与动脉粥样硬化、血钙、磷酸盐、血脂、甲状腺、甲状旁腺等因素有关的主动耗能,多因素调控的病理过程
To make clear the hypothesis , a middle cerebral artery occlusion ( mcao ) and hypoxia and glucose - deprivation ( hgd ) ischemic models were used in in vivo and in vitro study , respectively . we first studied the cellular localization of kvl . 2 and the co - localization of kvl . 2 protein and vegf receptors flk - 1 and flt - 1 , observed the effect of mcao on kvl . 2 expression and phosphrylation in the rat brain in vivo , then investigated the effect of vegf on ischemia / hypoxia cell damage and tyrosine phosphorylation of kvl . 2 in sh - sy5y cells . finally , in order to further elucidate the relationship between vegf ' s neuroprotection and its regulation on kvl . 2 phosphorylation , we used a specific antisense oligodeoxynucleotide ( odn ) to knockdown the expression of endogenous vegf to observe its role in ischemia / hypoxia cell damage and regulation of kvl . 2 phosphorylation 为了验证上述假设，本文分别在整体和离体水平，采用大脑中动脉缺血( middlecerebralarteryocclusion ， mcao )和体外氧?糖剥夺( hypoxiaandglucose - deprivation ， hgd )缺血模型，首先了解了kv1 . 2蛋白的细胞定位及与vegf受体flk - 1和flt - 1的共存情况，观察了整体mcao后缺血再灌不同时间大鼠脑内kv1 . 2蛋白的磷酸化水平变化，然后通过外源性给予vegf蛋白，在sh - sy5y细胞株上观察其对缺血细胞存活率及kv1 . 2蛋白磷酸化水平的影响，最后利用vegf反义脱氧寡核苷酸( oligodeoxynucleotide ， odn )特异阻断内源性vegf蛋白的表达，观察内源性vegf蛋白在缺血细胞损伤及调节kv1 . 2蛋白磷酸化中的作用，以进一步明确vegf缺血保护效应与其调节kv1 . 2蛋白磷酸化之间的关系。
