脑动脉瘤合并主动脉弓离断一例

患者 男,25岁.因突发剧烈头痛,以蛛网膜下腔出血收入院.颅脑CTA示后交通动脉瘤.平素体健.由右侧股动脉穿刺行伞脑血管造影,造影导管无法进入主动脉弓,只能进入左侧椎动脉和左侧的锁骨下动脉,推注造影剂,见到血液沿着椎动脉逆流入锁骨下动脉和降主动脉.然后,由右侧肱动脉穿刺置人造影导管,发现降主动脉是通过右侧的椎动脉,左侧椎动脉供血,属于b型主动脉弓离断(图1,2).     

DSA和TCD对兔蛛网膜下腔出血脑血管痉挛的评价

目的 探讨在小动物如兔蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)模型上经股动脉入路行选择性椎-基底动脉造影的可行性;探讨TCD对兔SAH后CVS状况的评价效度.方法 采用枕大池2次注血法建立兔迟发性CVS的动物模型.术前1 d和术后3、5 d行选择性脑血管造影,判断CVS的程度;术前1 d及术后1、3、 5、 7 d行TCD连续检测基底动脉血流速度,从而判断CVS的变化及程度.结果 在家兔CVS动物模型上成功完成左侧椎动脉选择性插管和造影,可有效地判断CVS的严重程度;采用TCD连续监测基底动脉血流速度可获得稳定图谱,能观察到制模后血流速度的变化情况.结论 经兔股动脉入路行选择性椎-基底动脉造影是完全可行的,TCD可连续监测兔基底动脉血流速度,对兔SAH后CVS状况的评价稳定可靠,TCD与脑血管造影在检测SAH后CVS方面具有良好相关性.     

iFlow成像技术对中脑周围非动脉瘤性蛛网膜下腔出血后脑血管痉挛的评估

目的 探讨iFlow成像技术在中脑周围非动脉瘤性蛛网膜下腔出血（PNSAH）后脑血管痉挛评估中的价值。方法 收集经CT及两次血管造影明确诊断为PNSAH 60例为观察组,收集我院同期颅内动脉瘤单纯弹簧圈栓塞治疗后半年以上随访复查造影时未见复发60例为对照组。利用西门子公司iFlow软件测量首次造影和复查造影时双侧颈内动脉分叉部、双侧大脑中动脉分叉部、双侧椎动脉造影基底动脉末端相同部位的造影剂达峰时间（TTP）。结果 与对照组相比,观察组首次造影中双侧椎-基底动脉末端造影剂TTP明显增高（P<0.05）,观察组复查造影中双侧椎-基底动脉末端、右侧颈内分叉部、右侧大脑中分叉部造影剂TTP均明显增高（P<0.05）。与首次造影相比,观察组复查造影双侧椎-基底动脉末端造影剂TTP明显增高（P<0.05）。结论 PNSAH后存在血管痉挛,且以基底动脉最明显,应用iFlow技术评估脑血管痉挛的具有可行性。     

脑池内局部应用尼卡地平多聚体缓释微球治疗脑血管痉挛的实验研究

目的 研究脑池内注入NC -PLGA缓释微球对脑血管痉挛的治疗作用.方法 采用枕大池二次注血法制作兔蛛网膜下腔出血模型.分别采用脑池内注入NC -PLGA微球和尼卡地平的方法治疗脑血管痉挛.应用经颅多普勒技术测基底动脉的血流速度,脑血管造影测量基底动脉直径,光镜和电镜行病理检查,观察基底动脉的形态学变化,评价脑血管痉挛的严重程度.结果 脑池内注入NC - PLGA微球和尼卡地平都能降低基底动脉的血流速度(P＜0.01),基底动脉的直径明显升高(P＜0.01),并能明显改善血管壁的病理改变,但前者只需一次性注入后者总量的1/4既可达到同样的疗效.结论 经脑池内注入NC -PLGA缓释微球能明显减轻脑血管痉挛的严重程度,并可减轻痉挛血管壁的病理学变化.     

股动脉经皮穿刺插管行椎动脉造影

椎动脉造影的方法很多,大致可分为两类:(1)直接穿刺椎动脉造影;(2)直接注射或插管于椎动脉以外的血管进行椎动脉造影。后者又有不同的方法,包括:①右颈总动脉逆行注射,显示右锁骨下动脉和右椎动脉;②主动脉弓造影,造影剂经各种途径注入主动脉弓,显示包括椎动脉在内的所有脑血管;③直接穿     

经股动脉插管行椎动脉造影37例分析(摘要)

本组股动脉插管为经皮穿刺者27例,切开显露股动脉者10例。除5例分别因插管不达锁骨下动脉及椎基动脉未显影外,32例造影成功。6例为导管插入椎动脉,余均置导管于左锁骨下动脉的椎动脉开口处后注入Conray显影剂。32例的左椎动脉、基底动脉及其主     

选择性脑血管造影技术在兔迟发性脑血管痉挛模型中的应用

目的 探讨在小动物如兔脑血管痉挛动物模型上经股动脉入路进行椎-基底动脉选择性插管和血管造影的可行性，为在椎动脉内选择性注入具有扩张血管功能的基因药物来防治脑血管痉挛奠定基础。方法 采用“枕大池2次注血法”建立兔迟发性脑血管痉挛的动物模型，在数字减影血管造影机示踪图指引下，应用超选择性导丝导向技术将微导管选择性插入痉挛兔左侧椎动脉内，进行选择性血管造影判断血管痉挛的程度。结果 在家兔脑血管痉挛动物模型上成功完成左侧椎动脉选择性插管和造影，可以有效地判断血管痉挛的严重程度，基底动脉病理学检查进一步证实血管痉挛的发生。结论 本研究表明微导管可以选择性插入血管痉挛兔的椎动脉内，应用此技术可进一步在兔血管痉挛动物模型上选择性动脉内注入具有扩张血管功能的物质。     

甲基强的松龙对兔实验性脑血管痉挛的作用

目的探讨大剂量甲基强的松龙对蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)的作用。方法将24只雄性新西兰白兔随机分成2组:SAH对照组和SAH 大剂量甲基强的松龙(MP,18mg/kg)治疗组。通过枕大池二次注血法构建SAH模型,观察MP对脑基底动脉的影响。应用酶联免疫生化技术检测各组兔基底动脉血管平滑肌细胞膜蛋白激酶C(PKC)活性。结果经脑血管造影证实该剂量甲基强的松龙明显减轻实验性脑血管痉挛的严重程度,与对照组相比,PKC活性在大剂量甲基强的松龙治疗组没有明显提高。结论大剂量甲基强的松龙能够明显减轻脑血管痉挛程度,通过抑制血管平滑肌细胞来防治脑血管痉挛的发生发展。     

甲基强的松龙对兔实验性脑血管痉挛的作用

目的探讨大剂量甲基强的松龙对蛛网膜下腔出血（SAH）后脑血管痉挛（CVS）的作用。方法将24只雄性新西兰白兔随机分成2组：SAH对照组和SAH＋大剂量甲基强的松龙（MP，18mg／kg）治疗组。通过枕大池二次注血法构建SAH模型，观察MP对脑基底动脉的影响。应用酶联免疫生化技术检测各组兔基底动脉血管平滑肌细胞膜蛋白激酶C（PKC）活性。结果经脑血管造影证实该剂量甲基强的松龙明显减轻实验性脑血管痉挛的严重程度，与对照组相比，PKC活性在大剂量甲基强的松龙治疗组没有明显提高。结论大剂量甲基强的松龙能够明显减轻脑血管痉挛程度，通过抑制血管平滑肌细胞来防治脑血管痉挛的发生发展。     

闭锁综合征临床与脑血管造影结果的对比研究

目的:研究椎一基底动脉系统缺血所致闭锁综合征的临床特点与全脑血管造影的情况。方法:对13例经MRI证实的双侧桥脑基底部梗塞的闭锁综合征患者行股动脉插管全脑血管造影术,观察脑供血障碍的情况,并给予静脉和动脉溶栓治疗。结果:13例患者死亡8例,存活5例,超早期静脉溶栓4例,效果不佳,早期动脉溶栓4例,2例闭塞的基底动脉再通,恢复较好。脑血管造影示双侧椎动脉起始部严重狭窄并扭曲2例,优势供血的椎动脉起始部严重狭窄1例,椎动脉V3段闭塞波及基底动脉下段2例,基底动脉起始段闭塞4例,基底动脉中段闭塞3例,基底动脉全程狭窄1例。结论:椎一基底动脉不同部位闭塞或严重狭窄可引起双侧桥脑基底部梗塞,表现为闭锁综合征,死亡率高,早期动脉溶栓有一定效果。     

动脉持续灌注大蒜素对兔脑血管痉挛的实验研究

目的　观察大蒜素对实验性蛛网膜下腔出血后脑血管痉挛的作用及影响。方法　将日本大耳白兔用“二次枕大池注血法”制作症状性脑血管痉挛模型。经一侧锁骨下动脉 ,用微量泵持续灌注大蒜素。结果　持续动脉灌注大蒜素 2天后 ,治疗组基底动脉直径比治疗前明显增大 (P<0 .0 1) ,神经系统损害症状级别明显降低 (P<0 .0 1) ;对照组均无明显改变 (P>0 .0 5 )。对照组基底动脉、脑组织缺血性损害病理改变较重 ,治疗组则无明显受损。结论　大蒜素对急性期脑血管痉挛有改善作用 ;并且动脉持续灌注大蒜素有预防迟发性脑血管痉挛作用     

Clentiazem protects against chronic cerebral vasospasm in rabbit basilar artery.

BACKGROUND AND PURPOSE: Experiments were carried out in rabbits to determine whether clentiazem (8-chlorodiltiazem), a cerebrovascular-selective calcium channel blocker, administered 24 hours before subarachnoid hemorrhage influenced the subsequent cerebral vasospasm. METHODS: Subarachnoid hemorrhage was induced by multiple injections of blood into the prepontine cisterns of 35 male New Zealand White rabbits, and clentiazem (5 mg/kg) was administered 4 times daily until sacrifice. Cerebral artery diameter was assessed in vivo by angiography. Functional features of basilar arteries were measured using conventional in vitro methodology. RESULTS: Clentiazem reduced the angiographic narrowing seen on days 2 and 5 from 35% and 34%, respectively (sham control, 1.42 +/- 0.31 mm [n = 22]), to 8% and 11%, respectively, and prevented the narrowing (32%) that occurred on day 9. Narrowing in the untreated rabbits was only partly reversed by papaverine; all narrowing in clentiazem-treated animals was papaverine sensitive. Clentiazem prevented or reduced many of the changes in the basilar artery caused by the subarachnoid hemorrhage. Of particular relevance to arterial narrowing were the increased wall stiffness, the transient spontaneous changes in wall force, and the reduction in relaxation to acetylcholine. Reduction of the changes in wall force induced by agonists and by stimulation of intramural sympathetic nerves was observed. CONCLUSIONS: The vascular damage associated with chronic cerebral vasospasm is related to calcium entry into the smooth muscle and endothelial cells, and possibly sympathetic nerve terminals, through calcium channels sensitive to clentiazem, which suggests that clentiazem may be of value in the management of chronic cerebral vasospasm.     

The effects of endothelin antagonist BQ-610 on cerebral vascular wall following experimental subarachnoid hemorrhage and cerebral vasospasm

Abstract. Endothelin, a potent vasoconstrictor, has been found to increase in the cerebrospinal fluid and serum of patients following subarachnoid hemorrhage (SAH) and to play a major role in the development of cerebral vasospasm. The aim of this study is to investigate the role of endothelin-A antagonist BQ-610 in the experimentally performed cerebral vasospasm following SAH. Thirty New Zealand rabbits were divided into three groups (each n = 10): group A, control group; Group B, SAH group; Group C, treatment (endothelin antagonist BQ-610 treated) group. In the study, the rabbits developed vasospasm after injection of intracisternal autolog blood into the cisterna magna. After cerebral vasospasm development, in group C, endothelin antagonist BQ-610 was injected intracisternally. Morphometrically, basilar artery lumen was constricted 25% and 62% compared to the control group (group A) in the endothelin treated group (group C) and the endothelin untreated group (group B), respectively. Histopathological findings of the basilar artery wall confirmed the therapeutic effect of endothelin antagonist in vasospasm development. Endothelin-A receptor antagonist BQ-610 has a therapeutic effect in the cerebral vasospasm following experimentally performed subarachnoid hemorrhage when used intracisternally.     

甘珀酸治疗蛛网膜下腔出血后脑血管痉挛的体内实验研究

目的 探讨缝隙连接抑制剂甘珀酸对实验性蛛网膜下腔出血后脑血管痉挛的治疗作用.方法 建立兔蛛网膜下腔二次出血模型,脑池及静脉分别给与缝隙连接抑制剂甘珀酸,脑血管造影及光镜观察分析基底动脉的直径及形态学变化,并应用Western blotting检测基底动脉Cx43蛋白的表达变化.结果 给与甘珀酸后,基底动脉狭窄程度及光镜下形态学变化显著减轻:单纯注血组(65.7±10.3)%,脑池处理组(91.2±6.4)%,静脉处理组(96.4±11.0)%,腑池预处理组(89.7±12.8)%;同时也显著抑制了痉孪后Cx43蛋白表达水平的升高:单纯注血组(57.2±2.8)%,脑池处理组(10.0±5.3)%,静脉处理组(15.2±1.7)%.结论 缝隙连接抑制剂甘珀酸可能对蛛网膜下腔出血后脑血管痉挛起到预防和治疗作用.     

甘珀酸对兔脑血管痉挛时缝隙连接蛋白43磷酸化表达的影响

目的 探讨甘珀酸对兔实验性蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)时缝隙连接蛋白43(Cx43)磷酸化表达的影响.方法 建立兔二次SAH模型,脑池及静脉分别给予甘珀酸,脑血管造影及光镜观察分析基底动脉直径及形态学变化并应用Western blot检测基底动脉Cx43蛋白磷酸化表达的变化.结果 SAH组与正常组相比,脑血管造影及光镜观察结果 证实基底动脉痉挛明显;痉挛动脉肇磷酸化的Cx43(P-Cx43)蛋白表达显著升高,但去磷酸化的Cx43(NP-Cx43)蛋白表达显著减少.甘珀酸脑池处理组及静脉处理组与SAH组相比,脑血管造影及光镜观察结果 证实基底动脉痉挛显著减轻;痉挛动脉壁P-Cx43蛋白表达显著减少,但NP-Cx43蛋白表达显著升高.结论 SAH后,Cx43蛋白磷酸化表达发生变化,脑池或静脉给予甘珀酸能明显缓解SAH后CVS,其作用机制可能与基底动脉Cx43蛋白磷酸化表达变化有关.     

Trapidil对蛛网膜下腔出血后脑血管痉挛作用的实验研究

目的 探讨蛛网膜下腔出血（SAH）后脑血管痉挛的发生机制及其可能的治疗方法。方法 利用家兔枕大池内注血构建SAH模型，观察血小板衍生生长因子（PDGF）拮抗剂trapidil对脑基底动脉的影响。结果 脑基底动脉于SAH后48h明显变细；静脉或动脉内持续灌注trapidil 15min（1．5mg／min）后，数字减影脑血管造影（DSA）显示痉挛血管已明显扩张变粗，30min时达高峰。结论 PDGF可能参与脑血管痉挛发生的病理过程，PDGF拮抗剂trapidil可有效缓解实验性SAH后脑血管痉挛，有望成为脑血管痉挛的治疗药物。     

Intrathecal application with liposome-entrapped Fasudil for cerebral vasospasm followingsubarachnoid hemorrhage in rats

To date, the pharmacological approach to cerebral vasospasm following subarachnoid hemorrhage has been hampered in part by an inability to attain sufficiently high concentrations of vasodilator drugs in the cerebrospinal fluid (CSF). To overcome this limitation of current drug therapy, we have developed a sustained-release preparation of protein kinase inhibitor Fasudil. Cerebral vasospasm in rats was induced by double-injection method. Treated rats received 0.417 mg liposome-entrapped Fasudil via the cisterna magna and control rats received drug-free liposomes in the same manner. The diameter of the basilar artery was assessed at 7 days after the initial blood injection. Vasoconstriction of the rat basilar artery was significantly reduced in group treated with liposomal Fasudil compared to the control group (treated group: 87.7 +/- 6.18%, n= 10; control group: 66.3 +/- 9.82%, n = 10; ***P< 0.001). This new approach for cerebral vasospasm may have significant potential for use in the clinical setting.     

实验性蛛网膜下腔出血后脑血管痉挛兔基底动脉Cx43蛋白表达的时相变化

目的 通过建立兔二次蛛网膜下腔出血实验模型,观察兔蛛网膜下腔出血后基底动脉缝隙连接蛋白Cx43表达的时相变化特点,初步探讨蛛网膜下腔出血后脑血管痉挛的形成机制.方法 选择健康新西兰大白兔30只,随机分为5组:正常对照组(n=6)和蛛网膜下腔出血模型组(1d、3d、7d和14d,n=6):建立兔二次蛛网膜下腔出血后脑血管痉挛实验模型,脑血管造影分析基底动脉的直径变化并应用Western Blot检测基底动脉Cx43蛋白的表达变化.对血管直径与Cx43表达变化情况进行相关分析.结果 成功建立兔二次蛛网膜下腔出血模型;脑血管造影显示注血后1d基底动脉即出现痉挛(85.7%±8.6%,P<0.05);7d时达高峰(66.5%±7.6%,P<0.01);14d时仍有痉挛(78.4%±8.2%,P<0.05)但程度较前缓解.Cx43蛋白表达在建立SAH模型后1d(38.6%±5.6%,P<0.05)、3d(50.2%±5.7%,P<0.05)、7d(57.8%±5.3%,P<0.01)、14d(32.4%±3.6%.P<00.05)均升高,其中7d为高峰,14d开始下降.Cx43蛋白表达的时相性变化与SAH后基底动脉直径的时相性变化相关系数为0.914.结论 实验结果 显示蛛网膜下腔出血后兔基底动脉缝隙连接蛋白Cx43的表达发生了时相性变化,并且Cx43蛋白表达强弱与蛛网膜下腔出血后脑血管痉挛程度在时程上存在正相关关系,表明缝隙连接蛋白Cx43可能参与蛛网膜下腔出血后脑血管痉挛的形成.

Abstract：

Objective The study was designed to explore the change of expression of connexin43(Cx43)protien in the model of subarachnoid hemorrhage(SAH)of rabbits,hoping to provide the basis to study the mechanism of cerebral vasospasm(CVS).Methods 30 New Zealand rabbits were divided into 5 groups:SAH group(1d,3d,7d,14d,n=6)and control group(n=6).The model of CVS following SAH was established.Digital subtraction angiography was performed to detect the change of the basilar arteries diameter.The expression of Cx43 protien in basilar arteries tissue at different time points following experimental SAH was examined by using western blotting analysis.The data were statistically analyzed using the bivariate correlations test.Results The model of SAH in rabbits was successfully established.All 30 rabbits were analyzed.Cerebral angiograms on 1d,3d,7d and 14d showed severe narrowing of the BAs,and on 7d showed the most narrowing and on 14d began to Relieve.Western blotting showed that the expression of Cx43 protein were detected in normal rabbit basilar arteries tissue.However,the expression of Cx43 protein increased gradually and significantly in models compared with that of control(P<0.05),which reached peak on 7d(P<0.01)and then decreased on 14d(P<0.05).There was positive correlation between expression of Cx43 and cerebral vasospasm.Conclusions The above results demonstrates at the first time that the Cx43 protein expression is altered after the SAH,and exhibits a time-dependent change.which might be connected with the development of CVS.In summary,our data demonstrates gap junctions may play an important role in the pathogenesis of cerebral vasospasm after SAH.     

Arterial spasm following perimesencephalic nonaneurysmal subarachnoid hemorrhage in a pediatric patient

Perimesencephalic nonaneurysmal hemorrhage is a benign form of subarachnoid hemorrhages. This entity is well recognized as a distinct type of subarachnoid hemorrhage in adults. However, perimesencephalic nonaneurysmal subarachnoid hemorrhage in pediatric patients is not well recognized. Angiographic changes such as vasospasm are uncommon in patients, especially in pediatric patients suffering from this type of hemorrhage. This case study reports a 12-year-old male who suffered from perimesencephalic nonaneurysmal subarachnoid hemorrhage. Cerebral carotid angiography performed on the tenth day of the posthemorrhagic period revealed severe vasospasm affecting the basilar artery. The patient, treated symptomatically, was discharged after improvement. One year later, magnetic resonance angiography revealed completely normal features.     

细胞色素C在兔蛛网膜下腔出血后脑血管痉挛中的作用

目的 观察兔蛛网膜下腔出血(SAH)后基底动脉细胞色素C(Cyt-C)的表达规律,以探讨其在细胞凋亡中的作用及与脑血管痉挛(CVS)的关系.方法 36只新西兰大白兔随机分为对照组(6只)和SAH组(30只).SAH组采用枕大池二次注血法建立兔CVS模型,对照组行枕大池二次注入生理盐水.应用苏木精-伊红染色观察基底动脉形态学变化,TUNEL法检测基底动脉上细胞凋亡情况,免疫组化检测基底动脉内皮细胞和平滑肌细胞的Cyt-C表达.结果 对照组基底动脉结构正常,偶见凋亡细胞和Cyt-C表达.SAH组基底动脉出现相应病理学改变,管腔狭窄呈双相期改变;基底动脉上细胞凋亡和Cyt-C表达均在SAH后增多,于第7天达高峰,第10天逐渐下降.与对照组比较,SAH组内各时间点基底动脉直径和Cyt-C表达差异均有统计学意义(P<0.05).结论 兔CVS模型的基底动脉中存在细胞凋亡,Cyt-C是启动细胞凋亡的重要因素,在CVS发生和发展过程中起重要作用.