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岩静脉离断动物模型的建立及岩静脉离断对兔脑组织的影响
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摘要
背景1929年,Dandy教授在其文章中插图展示了一支走行于桥小脑角区域并经三叉神经背侧汇入岩上窦的静脉,此静脉便是后来众所周知的岩静脉。岩静脉是非常重要且相对恒定的解剖标志,在涉及天幕以及桥小脑角区病变的手术中扮演重要角色。
     袁贤瑞教授回顾2004年6月至2007年10月进行的听神经瘤手术33例,其中2例手术中岩静脉被电凝处理,31例保护良好。31例岩静脉保护良好的患者术后恢复良好,2例电凝处理岩静脉的患者继发小脑出血性梗死并水肿;1例死亡,1例经后颅窝减压后病情好转。因此,袁贤瑞教授认为手术中应当妥善保护岩静脉,这一观点得到很多学者的支持;但亦有部分学者认为手术中离断岩静脉对术后效果影响不大。目前,文献中未查及关于岩静脉的动物实验研究。
     目的建立家兔单侧岩静脉离断(双极电凝烧灼后,显微剪剪断)动物模型,观察岩静脉离断后家兔脑组织病理结构、含水量、钠钾离子含量、SOD活力、MDA含量及AQP-4转录与表达。
     方法1选用健康家兔10只(雌雄不限),解剖分离其颈动脉及颈静脉,应用硅橡胶对新鲜家兔尸头进行灌注。解剖观察灌注好的家兔尸头标本,比较家兔与人类岩静脉的解剖结构。2健康成年家兔144只随机分成两组,即假手术组与岩静脉离断组。每组按处死时间点即手术操作后4h、8h、12h、24h、48h、72h分成六个亚组,每个亚组12只家兔。每个亚组中取6只获取标本后,干湿重法检测小脑及脑干组织含水量;原子火焰吸收分光光度法检测钠钾离子含量;黄嘌呤氧化酶法检测SOD活力;硫代巴比妥酸(TBA)法检测MDA含量,RT-PCR检测AQP-4mRNA转录。亚组中另外六只采用HE染色、尼氏染色及电镜观察脑组织病理结构改变;免疫组织化学检测AQP-4蛋白表达。
     结果
     1家兔尸头灌注血管色泽鲜艳,细小血管显示良好,解剖结构保留完整,其岩静脉解剖结构与人类相似。
     2含水量及钠钾离子含量:A小脑组织:假手术组各亚组脑组织含水量、钠钾离子含量无统计学差异(p>0.05);岩静脉离断后4h、8h、12h、24h组脑组织含水量、钠离子含量高于假手术组(p<0.05),岩静脉离断后4h、8h、12h、24h组脑组织钾离子含量低于假手术组(p<0.05);岩静脉离断后4h脑组织含水量、钠离子含量增加,8-12达高峰,持续至24小时(p<0.05),钾离子含量自4h降低,8-12小时降至最低(p<0.05)。B脑干组织:假手术组各亚组脑组织含水量、钠钾离子含量无统计学差异(p>0.05);岩静脉离断后4h脑组织含水量、钠离子含量高于假手术组(p<0.05),钾离子含量低于假手术组(p<0.05)。
     3小脑组织病理结构改变:假手术组小脑组织神经细胞结构基本正常,岩静脉离断后4h、8h、12h出现水肿,表现为细胞肿胀,尼氏体消失,神经细胞变性坏死等。脑干组织病理结构改变:岩静脉离断4h组出现细胞水肿,岩静脉离断组其余各亚组与假手术组病理结构基本正常。
     4 SOD活力检测:A小脑组织:假手术组之间SOD活力无统计学差异(p>0.05)岩静脉离断后4h、8h、12h、24h脑组织SOD活力低于假手术组(p<0.05)岩静脉离断后4h脑组织SOD活力下降,8-12至最低,持续至24小时(p<0.05)。B脑干组织:假手术组各亚组脑组织SOD活力无统计学差异(p>0.05)岩静脉离断后4h脑组织SOD活力低于假手术组(p<0.05)。
     5 MDA含量检测:A小脑组织:假手术组之间MDA含量无统计学差异(p>0.05)岩静脉离断后4h、8h、12h、24h脑组织MDA含量高于假手术组(p<0.05)岩静脉离断后4h脑组织MDA含量上升,8-12达高峰,48-72小时接近假手术组(p<0.05)。B脑干组织:假手术组各亚组脑组织MDA含量无统计学差异(p>0.05)岩静脉离断后4h脑组织MDA含量高于假手术组(p<0.05)。
     6 AQP-4转录与表达:A小脑组织:假手术组各亚组脑组织AQP-4转录及表达无统计学差异(p>0.05);岩静脉离断后4h、8h、12h、24h脑组织AQP-4转录与表达增强(p<0.05)。B脑干组织:假手术组各亚组脑组织AQP-4转录及表达无统计学差异(p>0.05):岩静脉离断后4h脑组织AQP-4转录及表达强于假手术组(p<0.05)。
     结论
     1家兔具有与人类相似的岩静脉结构及引流,从解剖学角度讲,家兔可用于建立岩静脉离断动物模型。
     2岩静脉离断组4h、8h、12h、24h亚组小脑组织含水量及钠离子含量较假手术对照组增加,钾离子含量降低。表明岩静脉离断引起钠钾ATP酶功能障碍,导致小脑组织水肿。
     3岩静脉离断导致家兔脑组织病理结构改变,此结构改变为可逆性。
     4岩静脉离断组4h、8h、12h、24h亚组小脑组织较假手术对照组小脑组织MDA含量增加,SOD活力下降。表明脑细胞代谢及功能障碍,清除氧自由基的能力下降。提示对抗氧自由基可能有助于脑组织功能恢复。
     5岩静脉离断组4h、8h、12h、24h亚组小脑组织AQP-4转录与表达较假手术组增强,说明AQP-4参与了脑水肿的形成与发展。提示抑制AQP-4的表达可能能够减轻岩静脉离断导致的脑水肿。
Back ground In 1929, professor Walter Dandy first pointed out the importance of the petrosal vein in connection with surgery for trigeminal neuralgia. His illustration showed a vein that coursed in the cerebellopontine angle rostral to the trigeminal nerve to drain into the superior petrosal sinus. Later, this common stem came to be identified as the petrosal vein. Petrosal vein is an important and relatively constant anatomical landmark. It also plays an important role in surgery for tentorial and cerebellopontine angle tumours.
     Professor Yuan Xianrui reviewed 33 cases of acoustic neuroma surgery carried since June 2004 to October 2007, including 2 cases(coagulated petrosal vein) and 31 cases (well protected petrosal vein). Four patients that petrosal vein was coagulated developed cerebellar hemorrhagic infarction. One patient died,1 patient was carried posterior fossa decompression and recovered. Thus, Professor Yuan Xianrui pointed out that petrosal vein should be protected during surgery. His view has been supported by many scholars; however, some scholars don't think that sacrifice of the petrosal vein has effect on the results of operation. There are no exact animal experiments about the consequences after mutilation of petrosal vein at present.
     Objective To establish unilateral petrosal vein mutilation (coagulation by bipolar, cut by micro scissor) model of rabbit. To observe the brain water content, sodium and potassium content, SOD activity, MDA content, AQP-4 transcription and expression and pathological changes of brain tissue after mutilation of petrosal vein.
     Methods 1) 10 rabbits (either sex), separate the carotid artery and jugular vein, perfuse fresh rabbit cadaver by silicone. Observe rabbit cadaveric head specimens, compare it's petrosal vein with human's.2) 144 healthy adult rabbits were randomly divided into two groups, namely sham operation group and petrosal vein mutilation group. Rabbits were killed at 4h,8h,12h,24h,48h,72h after operation. Groups were divided into six sub-groups according to the time points (n=12 in each sub-group). Six of each sub-group were taken to measure water content by the wet and dry weight method; the content of sodium and potassium by flame photometer, SOD activity by xanthine oxidase assay, MDA content by thiobarbituric acid (TBA) assay, AQP-4mRNA transcription by RT-PCR. The other six of each sub-group were taken to observe the brain tissue pathological changes by HE staining, Nissl staining and electron microscopy structure, AQP-4 protein expression by immunohistochemistry.
     Results
     1 Color of perfused vessels was bright, small blood vessels were clear, anatomical structures were remained well, the petrosal vein was similar to human's.
     2 Water content, sodium and potassium ion content:A) cerebellar tissues:brain water content, sodium and potassium ion content had no statistic difference in sham operation groups (p>0.05); water content and sodium content of 4h,8h,12h,24h sub-groups of petrosal vein mutilation group was higher than sham operation groups (p<0.05), potassium content of 4h,8h,12h,24h sub-groups of petrosal vein mutilation group were lower than the sham operation groups (p<0.05);4 hours after the mutilation of petrosal vein, water content and sodium content increased, they reached maximum 8-12 hours later, continued to 24 hours (p<0.05). Potassium ions content decreased to minimum 8-12 hours later (p<0.05). B) brain stem:water content, sodium and potassium ion content in sub-groups of sham operation group had no significant difference (p>0.05); 4 hours after mutilation of petrosal vein, brain water content, sodium content was higher than sham operation group (p<0.05), potassium content was lower than the sham operation group (p<0.05).
     3 Cerebellar pathological structural changes:structure of nerve cells of cerebellum were normal in sham operation groups; in 4h,8h,12h,24h sub-groups of petrosal vein mutilation group, the tissues appeared edema, manifested as cell swelling, disappearance of Nissl bodies, cell degeneration and necrosis. Pathological changes in the brain stem structure:4h sub-group of mutilation group show edema, pathological structures of the sham operation groups and other sub-groups of petrosal vein mutilation group were normal.
     4 SOD activity detection:A) cerebellum:SOD activity in the sham groups had no significant difference (p>0.05); SOD activity in 4h,8h, 12h,24h sub-groups of petrosal vein mutilation group were lower than in the sham operation groups (p<0.05); SOD activity decreased 4hours later,8-12 hours reached minimum, continued to 24 hours (p<0.05). B) brain stem:SOD activity had no significant difference in sham operation groups (p>0.05); SOD activity in 4h sub-group of petrosal vein mutilation group is lower than in sham operation group (p<0.05).
     5 MDA content detection:MDA content in the sham groups had no significant difference (p>0.05); MDA content in 4h,8h,12h,24h sub-groups of petrosal vein mutilation group were higher than in the sham operation groups (p<0.05); MDA content increased 4hours later, 8-12 hours reached maximum, continued to 24 hours (p<0.05). B) brain stem:MDA detection had no significant difference in sham operation groups(p>0.05); MDA content in 4h sub-group of petrosal vein mutilation group is higher than in sham operation group (p<0.05).
     6 AQP-4 transcription and expression:AQP-4 transcription and expression in the sham groups had no significant difference (p>0.05); AQP-4 transcription and expression in 4h,8h,12h,24h sub-groups of petrosal vein mutilation group were higher than in the sham operation groups (p<0.05); AQP-4 transcription and expression increased 4hours later,8-12 hours reached maximum, continued to 24 hours (p<0.05). B) brain stem:AQP-4 transcription and expression had no significant difference in sham operation groups(p>0.05); AQP-4 transcription and expression in 4h sub-group of petrosal vein mutilation group is higher than in sham operation group (p<0.05).
     Conclusions
     1 The structure and drainage of petrosal vein of rabbit was similar with human's, rabbits can be used to establish petrosal vein mutilation animal model.
     2 Compared with sham control group, cerebellar water content and sodium ion content increased in petrosal vein mutilation group, potassium content decreased. Mutilation of petrosal vein caused dysfunction of Na-K ATPase, resulted in cerebellar edema.
     3 Mutilation of petrosal vein can lead to pathological structural changes of rabbit brain tissues, the structural change is reversible.
     4 Compared with sham control group, MDA content increased in petrosal vein mutilation group, SOD activity decreased. Metabolism and function of neuron were damaged, the ability to eliminate oxygen free radicals decreased. Reduction of oxygen free radicals may contribute to brain function.
     5 Compared with sham control group, AQP-4 transcription and expression increased in petrosal vein mutilation group, indicating AQP-4 involved in the formation and development of cerebral edema. It suggested that inhibition of the expression of AQP-4 may be able to reduce brain edema.
引文
[1]Dandy W E. An operation for the cure of tic douloureux:partial section of the sensory root at the pons. Arch Surg,1929,18(2):687-734
    [2]Dandy W E.The trement of trigeminal neuralgia by cerebellar route.Annals of Surgery,1932,96(4):787-795
    [3]Braun J, Tournade A, Wackenheim A. The importance of normal venous landmarks in the topography of the mesencephalon, pons and cerebellum. Neuroradiology,1975,10(1):43-46
    [4]奚健,袁贤瑞,王君宇,等.听神经瘤手术中岩静脉的保护及其意义.中华神经外科杂志,2009,25(4):301-303
    [5]McLaughlin MR, Jannetta PJ, Clyde BL,et al.Microvascular decompression of cranial nerves:Lessons learned after 4400 operations.J Neurosurg,1999,90 (1):1-8
    [6]Gharabaghi A,Koerbel A,Lowenheim H. The impact of petrosal vein preservation on postoperative auditory function in surgery of petrous apex meningiomas.Neurosuegery,2006,59(1):S68-74
    [7]Zhong J,Li ST,XuSQ,et al.Management of petrosal veins during microvascular decompression for trigeminal neuralgia.Neurological Research,2008,30(7): 697-700
    [8]焦迎斌,丰育功.微血管减压术中岩静脉切断的可行性研究.中国临床神经外科杂志,2007 12(10):610-613
    [9]Gotoh M, Ohmoto T, Kuyama H. Experimental study of venous circulatory disturbance by dural sinus occlusion. Acta Neurochir,1993,124(2):120-126
    [10]Fries G, Wallenfang T, Hennen J, et al. Occlusion of the pig superior sagittal sinus, bridging and cortical veins:multistep evolution of sinus-vein thrombosis. J Neurosurg,1992,77(1):127-133
    [11]Nakase H, Nagata K, Otsuka H, et al. Local cerebral blood flow autoregulation following "asymptomatic" cerebral venous occlusion in the rat. J Neurosurg,1998,89(1):118-124
    [12]MC Papadopoulos, S Krishna,AS Verkman. Aquaporin Water Channels and Brain Edema. Mount Sinai Journal of Medicine,2002,69:242-248
    [13]Masuoka J,Matsushima T,Hikita T. Cerebellar swelling after sacrifice of the superior petrosal vein during microvascular decompression for trigeminal neuralgia.Journal of Clinical Neuroscience,2009,16(10):1342-1344
    [14]漆光平,杜亚政,潘爱华,等.乳胶血管灌注的技术探讨.湖南医科大学学报,2000,25(4):411-412
    [15]郝少才,徐军,夏鹤春.硅橡胶灌注制作头颈部血管标本的技术.宁夏医学院学报,2006,28(4):358-359
    [16]Leonhard T, Lehmann R. The petrosal vein and its demonstration in the normal vertebral angiogram. Neuroradiology,1976,10(5):271-275
    [17]Rhoton Al Jr. The postetior fossa veins.Neurosurgery,2000,47(3):S69-92
    [18]Matsushima T, Rhoton AL Jr, de Oliveira E, et al.Microsurgical anatomy of the veins of the posterior fossa. J Neurosurg,1983,59(1):63-105
    [19]Necmettin T,Hiroshi A, Rhoton AL Jr,et al.Microsurgical anatomy of the superior petrosal venous complex:new classifications and implications for subtemporal transtentorial and retrosigmoid suprameatal approaches. J Neurosurg,2007,106(6):1041-1050
    [20]蒋吉英,高培福,窦寰宇,等.岩静脉的解剖学特征及临床意义.中国临床解剖学杂志,1999,17(1):34-35
    [21]张继志,段云平,高宝山,等.岩静脉的显微解剖研究及术中处理.中国微创外科杂志,2008,8(8):713-715
    [22]M Braun,S Bracard,J-C Huot.Pontine veins.MRI cross-sectional anatomy. Surg Radiol Anat,1996,18(4):315-321
    [23]Guppy KH, Origitano TC, Reichman OH, et al.Venous drainage of the inferolateral temporal lobe in relationship to transtemporal/transtentorial approaches to the cranial base. Neurosurgery,1997,41(3):615-620
    [24]Sakata K, Al-Mefty O, Yamamoto I. Venous consideration in petrosal approach: Microsurgical anatomy of the temporal bridging vein. Neurosurgery,2000,47 (1):153-161
    [25]Ungersbock K, Heimann A, Kempski O, et al. Cerebral blood flow alterations in a rat model of cerebral sinus thrombosis. Stroke,1993,24:563-569
    [26]Nakase H, Heimann A, Kempski O. Alteration of regional cerebral blood flow and oxygen saturation in a rat sinus-vein thrombosis model. Stroke,1996,27 720-728
    [27]Hossmann KA,Schuier FJ.Experimental brain infarcts in cats.Ⅰ.Pathophysiolog-ical observations. Stroke,1980,11(6):583-592
    [28]Koerbel A,Gharabaghi A,Safavi-Abbasi S,et al. Venous complications following petrosal vein sectioning in surgery of petrous apex meningiomas.Eur J Surg Oncol,2009,35(7):773-779
    [29]Inamasu J,Shiobara R,Kawase T. Haemorrhagic venous infarction following the posterior petrosal approach for acoustic neurinoma surgery:a report of two cases.Eur Arch Otorhinolaryngol,2002 259(3):162-165
    [30]Singh D,Jagetia A,Sinha S. Brain stem infarction:A complication of microvascular decompression for trigeminal neuralgia.Neurology India,2006,54(3):325-326
    [31]RyU H,Yamamoto S,Sugiyama K,et al.Neurovascular decompression for trigeminal neuralgia in elderly patients.Neurol Med Chir (Tokyo),1999,39(3): 226-230
    [32]Koerbel A,Wolf SA,Kiss A. Peduncular hallucinosis after sacrifice of veins of the petrosal venous complex for trigeminal neuralgia.Acta Neurochir(Wien), 2007,149(8):831-833
    [33]Tsukamoto H, Matsushima T, Fujiwara S,et al. Peduncular hallucinosis following microvascular decompression for trigeminal neuralgia:case report. Surg Neurol,1993,40(1):31-34
    [34]Strauss C,Naraghi R,Bischoff B. Contralateral hearing loss as an effect of venous congestion at the ipsilateral inferior colliculus after microvascular decompression:report of a case. J Neurol Neurosurg Psychiatry 2000,69(5):679-682
    [35]沈同.生物化学.北京:高等教育出版社,1990.428
    [36]Macdonald RL,Stoodley M.Pathophysiology of Cerebral Ischemia.Neurol Med Chi(Tokyo),1998,38:1-11
    [37]Nemoto EM,Hossmann KA,Cooper HK.Post-ischemic hypermetabolism in cat brain.Stroke,1981,12:666-676
    [38]武忠弼.超微病理诊断学.上海:上海科技出版社,2003.397
    [39]Romansky K, Stamenov B. Ultrastructural study of cerebral cortex and subcortical white matter following ligation of bridging veins in cats. Zentralbl Neurochir,1995,56(3):111-116
    [40]张思讯,左焕琼.大鼠上矢状窦后1/3夹闭对其回流区组织的影响.中华创伤杂志,1995,11(4):219-220
    [41]唐忠,袁贤瑞,姜维喜,等.家兔上矢状窦中1/3及其回流静脉结扎动物模型的建立.中国微侵袭神经外科杂志,2006,11(3):123-125
    [42]Mecord JM.Oxygen-derived free radicals in postischemic tissue injury. NEnglMed,1985,312:159-163
    [43]Li J, Verkman A S. Impaired hearing in mice lacking aquaporin-4 water channels. J Biol Chem,2001,276(33):31233-31237
    [44]Manley G T, Fujimura M, Ma T, et al. Aquaporin-4 deletion in mice reduces brain edema after acute water intoxication and ischemic stroke. Nat Med,2000, 6(2):159-163.
    [45]Nicchia G P, Frigeri A, Liuzzi G M, et al. Inhibition of aquaporin-4 expression in astrocytes by RNAi determines alteration in cell morphology, growth, and water transport and induces changes in ischemia-related genes. FASEBJ,2003, 17(11):1508-1010
    [46]Kenneth J. L, Thomas D. S. Analysis of relative gene expression data using real-time quantitative PCR and the 2ΔΔCT method.METHODS,2001,25(4): 402-408
    [47]Halliwell B,Gutteridge JMC.Free Radicals in Biology and Medicine.2nd ed.Oxord:Clarendon Press,1989.121
    [48]叶琳,龚书明,陈耀明,等.次声作用对大鼠大脑皮层脂质过氧化的影响.中华物理医学与康复杂志,2002,24(6):360-362
    [49]孙树清,吴中学,张友平,等.脑损伤后组织自由基变化的实验研究.首都医科大学学报,2002,23(3):236-239
    [50]Hara H,Sukamoto T, Kogure K.Mechanism and pathogenesis of ischemia-induced neorunal damage.Progress in Neorubiology,1993,40(6): 645-670
    [51]Atsushi S; Hideyuki K, Ichiro K,et al.Transgenic CuZn-superoxide dismutase inhibits NO synthase induction in experimental subarachnoid hemorrhage.Stroke,2001,32:1652-1657
    [52]Simonian NA,Coyle JT.Oxidative stress in neurodegenerative diseases.Annual Review of Pharmacology angd Toxicology,1996,36:83-106
    [53]Zhan H, Lu JY, Zhang QJ, et al.Protective effects of tea Polyphenols on mild hypobairic hypoxia induced Pulmonary free radical metabolic disorder in mice.Space Med Eng,2001,14(2):79-83.
    [54]Denker BM, Smith BL, Kuhajda FP,et al.Identification, purification, and partial characterization of a novel Mr 28,000 integral membrane protein from erythrocytes and renal tubules. J Biol Chem,1988,263:15634-15642
    [55]Jung JS, Bhat RV, Preston GM, Guggino WB, et al. Molecular characterization of an aquaporin cDNA from brain:candidate osmoreceptor and regulator of water balance. Proc. Natl.Acad. Sci. USA,1994,91 (26):13052-13056
    [56]Badant J, Lasbennes F, Magistretti PJ, et al. Aquaporins in brain distributions, physiology, and pathophsiology:International Society of cerebral. Blood Flow and Metabolism,2002,44(26):367-378
    [57]Nakahama K, Fujioka A, Nagano M, et al. A role of the c-terminus of aquaporin-4 in its membrane expression in cultural astrocytes. Genes to cells,2002,7(22):731-733
    [58]Frigeri A, Gropper MA, Turck CW, et al. Immunolocalization of the mercurial-insensitive water channel and glycerol intrinsic protein in epithelial cell plasma membranes. Proc. Natl. Acad. Sci. USA,1995,92:4328-4331
    [59]Frigeri A, Gropper MA, Umenishi F,et al. Localization of MIWC and GLIP water channel homologs in neuromuscular, epithelial and glandular tissues. J. Cell Sci,1995,108(9):2993-3002
    [60]Frigeri A, Nicchia GP, Verbavatz JM,et al. Expression of Aquaporin-4 in fast-twitch fibers of mammalian skeletal muscle. J. Clin. Invest,1998,102(4): 695-703
    [61]Nielsen S, King LS, Christensen BM, et al. Aquaporins in complex tissues. Ⅱ. Subcellular distribution in respiratory and glandular tissues of rat. Am. J. Physiol,1997,273(5):c 1549-c 1561
    [62]Nielsen S, Nagelhus EA, Amiry-Moghaddam M,et al. Specialized membrane domains for water transport in glial cells:high-resolution immunogold cytochemistry of aquaporin-4 in rat brain. J. Neurosci,1997,17(1):171-180
    [63]Hamann S, Zeuthen T, M La Cour,et al. Aquaporins in complex tissues: distribution of aquaporins 1-5 in human and rat eye. Am. J. Physiol,1998,274(5): c1332-c1345
    [64]Mhatre AN, Stern RE, Li J,et al. Aquaporin 4 expression in the mammalian inner ear and its role in hearing. Biochem. Biophys. Res. Commun,2002,297(4): 987-996
    [65]Oshio K, Watanabe H, Song Y,et al. Reduced cerebrospinal fluid production and intracranial pressure in mice lacking choroid plexus water channel Aquaporin-1 FASEB J,2005,19:76-78
    [66]Badaut J, Hirt L, Granziera C,et al.Astrocyte-specific expression of aquaporin-9 in mouse brain is increased after transient focal cerebral ischemia.J Cereb Blood Flow Metab 2001,21:477-482
    [67]Elkjaer M, Vajda Z, Nejsum LN,et al.Immunolocalization of AQP9 in liver, epididymis, testis, spleen, and brain. Biochem Biophys Res Commun,2000,276(3):1118-1128
    [68]Lee MD, King LS, Agre P. The Aquaporin family of water channel proteins in clinical medicine. Medicine,1997,76(4):141-156
    [69]Badaut J, Verbavatz JM, Freund-Mercier MJ, et al. Presence of aquaporin-4 and muscarinic receptors in astrocytes and ependymal cells in rat brain:a clue to a common function?. Neurosci Lett,2000,292(2):75-78
    [70]Amiry-Noghaddam M, Xue R, Haug FM, et al. Alpha syntuophin deletion removes the perivasular but not endothelial pool of aquaporin-4 at the blood-brain barrier and delays the development of brain edema in an experimental model of acute hyponatremia. FASEB J,2004,18(3):542-544
    [71]Saadoun S, Papadopoulos MC, Davies DC, et al.Aquaporin-4 expression is increased in oedematous human brain tumours. J Neurol Neurosurg Psychiatry,2002,72:262-265
    [72]Warth A, Kroger S, Wolburg H. Redistribution of aquaporin-4 in human glioblastoma correlates with loss of agrin immunoreactivity from brain capillary basal laminae. Acta Neuropathol,2004,107(4):311-318
    [73]Papadopoulos MC, Verkman AS. Aquaporin-4 gene disruption in mice reduces brain swelling and mortality in pneumococcal meningitis. J Biol Chem,2005, 280:13906-13912
    [74]Badaut J, Brunet JF, Grollimund L, et al.Aquaporin 1 and aquaporin 4 expression in human brain after subarachnoid hemorrhage and in peritumoral tissue. Acta Neurochir Suppl,2003,86:495-498
    [75]Taniguchi M, Yamashi ta T, Kumura E,et al. Induction of aquaporin-4 water channel mRNA after focal cerebral ischemia in rats.Brain Res Mol Brain Res, 2002,78(12):131-137
    [76]Zeng HK, Wang QS, Deng YY, et al.Hypertonic saline ameliorates cerebral edema through downregulation of aquaporin-4 expression in the astrocytes. Neuroscience,2010,166(3):878-885
    [77]Manley GT, Fujimura M, Ma T, et al.Aquaporin-4 deletion in mice reduces brain edema after acute water intoxication and ischemic stroke. Nat Med,2000, 6:159-163
    [78]Yang B, Zador Z, Verkman AS. Glial cell aquaporin-4 overexpression in transgenic mice accelerates cytotoxic brain swelling. J Biol Chem,2008,283: 15280-15286
    [79]Amiry-Moghaddam M, Williamson A, Palomba M,et al. Delayed K+ clearance associated with aquaporin-4 mislocalization:phenotypic defects in brains of alpha-syntrophin-null mice. Proc Natl Acad Sci U S A,2003,100:13615-13620
    [80]Amiry-Moghaddam M, Frydenlund DS, Ottersen OP.Anchoring of aquaporin-4 in brain:molecular mechanisms and implications for the physiology and pathophysiology of water transport.Neuroscience,2004,129(4):999-1010
    [81]Zeynalov E, Chen CH, Froehner SC, et al.(2008) The perivascular pool of aquaporin-4 mediates the effect of osmotherapy in postischemic cerebral edema. Crit Care Med,2008,36(9):2634-2640
    [82]Papadopoulos MC, Manley GT, Krishna S,et al.Aquaporin-4 facilitates reabsorption of excess fluid in vasogenic brain edema. FASEB J,2004,18:1291-1293
    [83]Bloch O, Papadopoulos MC, Manley GT,et al. Aquaporin-4 gene deletion in mice increases focal edema associated with staphylococcal brain abscess. J Neurochem,2005,95(1):254-262
    [84]Bloch O, Auguste KI, Manley GT,et al. Accelerated progression of kaolin-induced hydrocephalus in aquaporin-4-deficient mice. J Cereb Blood Flow Metab,2006,26:1527-1537
    [85]Papadopoulos MC, Binder DK, Verkman AS. Enhanced macromolecular diffusion in brain extracellular space in mouse models of vasogenic edema measured by cortical surface photobleaching.FASEB J,2005,19:425-427
    [86]Amiry-Moghaddam M, Otsuka T, Hum PD, et al. An alpha-syntrophin-depend-ent pool of AQP4 in astroglial end-feet confers bidirectional water flow between blood and brain. Proc Natl Acad Sci U S A,2003,100:2106-2111
    [87]Tait MJ, Saadoun S, Bell BA, et al. Water movements in the brain:role of aquaporins. Trends Neurosci,2008,31(1):37-43
    [88]唐忠,袁贤瑞,粟枫,等.家兔上矢状窦中1/3及其回流静脉结扎后脑水肿变化和水通道蛋白-4表达的研究.中国神经精神疾病杂志,2005,31(6):405-408
    [89]孙国柱,张庆俊,赵宗茂,等.新西兰兔脊髓内水通道蛋白-4的定位与表达.第四 军医大学报,2006,27(24):2235-2238
    [90]Song Y,Ma T,Matthay MA, et al. Role of aquaporin-4 in airspace-to-capillary water permeability in intact mouse lung measured by a novel gravimetric method. J Gen Physiol,2000,115:17-27
    [91]Tang Y, Cai D, Chen Y. Thrombin inhibits aquaporin-4 expression through protein kinase C-dependent pathway in cultured astrocytes.J Mol Neurosci,2007, 31(1):83-93
    [1]Dandy W E. An operation for the cure of tic douloureux:partial section of the sensory root at the pons. Arch Surg,1929,18(2):687-734
    [2]Dandy W E.The trement of trigeminal neuralgia by cerebellar route.Annals of Surgery,1932,96(4):787-795
    [3]Braun J, Tournade A, Wackenheim A. The importance of normal venous landmarks in the topography of the mesencephalon, pons and cerebellum. Neuroradiology,1975,10(1):43-46
    [4]Guppy KH, Origitano TC, Reichman OH, et al.Venous drainage of the inferolateral temporal lobe in relationship to transtemporal/transtentorial approaches to the cranial base. Neurosurgery,1997,41(3):615-620
    [5]Sakata K, Al-Mefty O, Yamamoto I. Venous consideration in petrosal approach: Microsurgical anatomy of the temporal bridging vein. Neurosurgery,2000, 47(1):153-161
    [6]奚健,袁贤瑞,王君宇,等.听神经瘤手术中岩静脉的保护及其意义.中华神经外科杂志,2009,25(4):301-303
    [7]Leonhard T, Lehmann R. The petrosal vein and its demonstration in the normal vertebral angiogram. Neuroradiology,1976,10(5):271-275
    [8]Bull J, Kozlowski P. The angiographic pattern of the petrosal veins in the normal and pathological conditions. Neuroradiology,1970, 1(1):20-26
    [9]Perese D. Superficial veins of the brain from a surgical point of view. J Neurosurg,1960,17(3):402-412
    [10]Rhoton Al Jr. The postetior fossa veins.Neurosurgery,2000,47(3):S69-92
    [11]Fujimaki T, Kirini T. Coagulation of the petrosal vein for MVD. J Neurosurg,1999,90(6):1148
    [12]McLaughlin MR, Jannetta PJ, Clyde BL,et al.Microvascular decompression of cranial nerves:Lessons learned after 4400 operations. J Neurosurg,1999,90(1): 1-8
    [13]Matsushima T, Rhoton AL Jr, de Oliveira E, et al.Microsurgical anatomy of the veins of the posterior fossa. J Neurosurg,1983,59(1):63-105
    [14]Necmettin T,Hiroshi A, Rhoton AL Jr,et al.Microsurgical anatomy of the superior petrosal venous complex:new classifications and implications for subtemporal transtentorial and retrosigmoid suprameatal approaches. J Neurosurg,2007,106(6):1041-1050
    [15]蒋吉英,高培福,窦寰宇,等.岩静脉的解剖学特征及临床意义.中国临床解剖学杂志,1999,17(1):34-35
    [16]张继志,段云平,高宝山,等.岩静脉的显微解剖研究及术中处理.中国微创外科杂志,2008,8(8):713-715
    [17]焦迎斌,丰育功.微血管减压术中岩静脉切断的可行性研究.中国临床神经外科杂志,2007 12(10):610-613
    [18]M Braun,S Bracard,J-C Huot.Pontine veins.MRI cross-sectional anatomy.Surg Radiol Anat,1996,18(4):315-321
    [19]Yun Peng Huang, Bernard S,Sanford P.The veins of the posterior fossa-anterior or petrosal draining group.American Journal of Roentgenology,1968,104 (1): 36-56
    [20]Tsukamoto H, Matsushima T, Fujiwara S,et al. Peduncular hallucinosis following microvascular decompression for trigeminal neuralgia:case report. Surg Neurol,1993,40(1):31-34
    [21]Koerbel A,Wolf SA,Kiss A. Peduncular hallucinosis after sacrifice of veins of the petrosal venous complex for trigeminal neuralgia.Acta Neurochir(Wien), 2007,149(8):831-833
    [22]Strauss C,Naraghi R,Bischoff B. Contralateral hearing loss as an effect of venous congestion at the ipsilateral inferior colliculus after microvascular decompression:report of a case. J Neurol Neurosurg Psychiatry,2000, 69(5):679-682
    [23]Gharabaghi A,Koerbel A,Lowenheim H. The impact of petrosal vein preservation on postoperative auditory function in surgery of petrous apex meningiomas.Neurosuegery,2006,59(1):S68-74
    [24]Masuoka J,Matsushima T,Hikita T. Cerebellar swelling after sacrifice of the superior petrosal vein during microvascular decompression for trigeminal neuralgiaJournal of Clinical Neuroscience,2009,16(10):1342-1344
    [25]Inamasu J,Shiobara R,Kawase T. Haemorrhagic venous infarction following the posterior petrosal approach for acoustic neurinoma surgery:a report of two cases.Eur Arch Otorhinolaryngol,2002 259(3):162-165
    [26]Singh D,Jagetia A,Sinha S. Brain stem infarction:A complication of microvascular decompression for trigeminal neuralgia.Neurology India,2006,54 (3):325-326
    [27]Koerbel A,Gharabaghi A,Safavi-Abbasi S,et al. Venous complications following petrosal vein sectioning in surgery of petrous apex meningiomas.Eur J Surg Oncol,2009,35(7):773-779
    [28]Krespi Y, Gurol ME, Coban O, et al.Venous infarction of brainstem and cerebellum. J Neuroimaging,2001,11(4):425-431
    [29]Strauss C,Neu M,Bischoff B,et al.Clinical and Neurophysiological Observations after Superior Petrosal Vein Obstruction during Surgery of the Cerebellopontine Angle:Case Report.Neurosurgery,2001,48(5):1157-1161
    [30]Zhong J,Li ST,XuSQ,et al.Management of petrosal veins during microvascular decompression for trigeminal neuralgia.Neurological Research,2008,30(7): 697-700
    [31]RyU H,Yamamoto S,Sugiyama K,et al.Neurovascular decompression for trigeminal neuralgia in elderly patients.Neurol Med Chir (Tokyo),1999,39(3): 226-230
    [1]MC Papadopoulos, S Krishna,AS Verkman. Aquaporin water channels and brain edema. Mount Sinai Journal of Medicine,2002,69:242-248
    [2]Prough DS, Lang J.Therapy of patients with head injuries:key parameters for management. The Journal of trauma,1997,42:S10-S18
    [3]Roberts I, Schierhout G, Alderson P.Absence of evidencefor the effectiveness of five interventions routinely used in the intensive care management of severe head injury:a systematic review. Journal of Neurology,1998,65:729-733
    [4]Denker BM, Smith BL, Kuhajda FP,et al.Identification, purification, and partial characterization of a novel Mr 28,000 integral membrane protein from erythrocytes and renal tubules. J Biol Chem,1988,263:15634-15642
    [5]Agre P, Sasaki S, Chrispeels MJ. Aquaporins:a family of water channel proteins. Am. J. Physiol,1993,265:F461
    [6]Jung JS, Bhat RV, Preston GM, Guggino WB, et al. Molecular characterization of an aquaporin cDNA from brain:candidate osmoreceptor and regulator of water balance. Proc. Natl.Acad. Sci. USA,1994,91(26):13052-13056
    [7]Badant J, Lasbennes F, Magistretti PJ, et al. Aquaporins in brain distributions, physiology, and pathophsiology:International Society of cerebral. Blood Flow and Metabolism,2002,44(26):367-378
    [8]Nakahama K, Fujioka A, Nagano M, et al. A role of the c-terminus of aquaporin-4 in its membrane expression in cultural astrocytes. Genes to cells,2002,7(22):731-733
    [9]Neely JD, Nielsen S, Agre P, et al. Heterotetrameric composition of aquaporin-4 water channels. Biochemistry,1999,38(34):11156-11163
    [10]Frigeri A, Gropper MA, Turck CW, et al. Immunolocalization of the mercurial-insensitive water channel and glycerol intrinsic protein in epithelial cell plasma membranes. Proc. Natl. Acad. Sci. USA,1995,92:4328-4331
    [11]Frigeri A, Gropper MA, Umenishi F,et al. Localization of MIWC and GLIP water channel homologs in neuromuscular, epithelial and glandular tissues. J. Cell Sci,1995,108(9):2993-3002
    [12]Frigeri A, Nicchia GP, Verbavatz JM,et al. Expression of Aquaporin-4 in fast-twitch fibers of mammalian skeletal muscle. J. Clin. Invest,1998,102(4): 695-703
    [13]Nielsen S, King LS, Christensen BM, et al. Aquaporins in complex tissues. II. Subcellular distribution in respiratory and glandular tissues of rat. Am. J. Physiol,1997,273(5):C1549-c1561
    [14]Nielsen S, Nagelhus EA, Amiry-Moghaddam M,et al. Specialized membrane domains for water transport in glial cells:high-resolution immunogold cytochemistry of aquaporin-4 in rat brain. J. Neurosci,1997,17(1):171-180
    [15]Hamann S, Zeuthen T, M La Cour,et al. Aquaporins in complex tissues: distribution of aquaporins 1-5 in human and rat eye. Am. J. Physiol,1998,274(5): C1332-c1345
    [16]Mhatre AN, Stern RE, Li J,et al. Aquaporin 4 expression in the mammalian inner ear and its role in hearing. Biochem. Biophys. Res. Commun,2002,297(4): 987-996
    [17]Oshio K, Watanabe H, Song Y,et al. Reduced cerebrospinal fluid production and intracranial pressure in mice lacking choroid plexus water channel Aquaporin-1.FASEB J,2005,19:76-78
    [18]Badaut J, Hirt L, Granziera C,et al.Astrocyte-specific expression of aquaporin-9 in mouse brain is increased after transient focal cerebral ischemia.J Cereb Blood Flow Metab,2001,21:477-482
    [19]Elkjaer M, Vajda Z, Nejsum LN,et al.Immunolocalization of AQP9 in liver, epididymis, testis, spleen, and brain. Biochem Biophys Res Commun,2000, 276(3):1118-1128
    [20]Lee MD, King LS, Agre P. The Aquaporin family of water channel proteins in clinical medicine. Medicine,1997,76(4):141-156
    [21]Badaut J, Verbavatz JM, Freund-Mercier MJ, et al. Presence of aquaporin-4 and muscarinic receptors in astrocytes and ependymal cells in rat brain:a clue to a common function?. Neurosci Lett,2000,292(2):75-78
    [22]Amiry-Noghaddam M, Xue R, Haug FM, et al. Alpha syntuophin deletion removes the perivasular but not endothelial pool of aquaporin-4 at the blood-brain barrier and delays the development of brain edema in an experimental model of acute hyponatremia. FASEB J,2004,18(3):542-544
    [23]Manley GT, Fujimura M, Ma T, et al.Aquaporin-4 deletion in mice reduces brain edema after acute water intoxication and ischemic stroke. Nat Med,2000,6:159-163
    [24]Papadopoulos MC, Manley GT, Krishna S,et al.Aquaporin-4 facilitates reabsorption of excess fluid in vasogenic brain edema. FASEB J,2004,18:1291-1293
    [25]Bloch O, Auguste KI, Manley GT,et al. Accelerated progression of kaolin-induced hydrocephalus in aquaporin-4-deficient mice. J Cereb Blood Flow Metab,2006,26:1527-1537
    [26]Bloch O, Papadopoulos MC, Manley GT,et al. Aquaporin-4 gene deletion in mice increases focal edema associated with staphylococcal brain abscess. J Neurochem,2005,95(1):254-262
    [27]Binder DK, Oshio K, Ma T,et al. Increased seizure threshold in mice lacking aquaporin-4 water channels. Neuroreport,2004,15(2):259-262
    [28]Binder DK, Papadopoulos MC, Haggie PM, et al.In vivo measurement of brain extracellular space diffusion by cortical surface photobleaching. J Neurosci,2004,24(37):8049-8056
    [29]Binder DK, Yao X, Zador Z,et al.Increased seizure duration and slowed potassium kinetics in mice lacking aquaporin-4 water channels,Glia.2006, 53(6):631-636
    [30]Zador Z, Magzoub M, Jin S,et al. Microfiberoptic fluorescence photobleaching reveals size-dependent macromolecule diffusion in extracellular space deep in brain. FASEB J,2008,22:870-879
    [31]Amiry-Moghaddam M, Williamson A, Palomba M,et al. Delayed K+ clearance associated with aquaporin-4 mislocalization:phenotypic defects in brains of alpha-syntrophin-null mice. Proc Natl Acad Sci U S A,2003,100:13615-13620
    [32]Saadoun S, Papadopoulos MC, Hara-Chikuma M,et al. Impairment of angiogenesis and cell migration by targeted aquaporin-1 gene disruption. Nature,2005,434:7S6-792
    [33]Saadoun S, Papadopoulos MC, Watanabe H, et al. Involvement of aquaporin-4 in astroglial cell migration and glial scar formation. J Cell Sci,2005,118:5691-5698
    [34]Auguste KI, Jin S, Uchida K,et al.Greatly impaired migration of implanted aquaporin-4-deficient astroglial cells in mouse brain toward a site of injury. FASEB J,2007,21:108-116
    [35]Verkman AS, Hara-Chikuma M, Papadopoulos MC.Aquaporins-new players in cancer biology. J Mol Med,2008,86(5):523-529
    [36]Shapiro K, Marmarou A, Shulman K,et al.Characterization of clinical CSF dynamics and neural axis compliance using the pressure-volume index:Ⅰ. The normal pressure-volume index. Ann Neurol,1980,7:508-514
    [37]Klatzo I. Evolution of brain edema concepts. Acta Neurochir Suppl (Wien),1994, 60:3-6
    [38]Papadopoulos MC, Binder DK, Verkman AS. Enhanced macromolecular diffusion in brain extracellular space in mouse models of vasogenic edema measured by cortical surface photobleaching.FASEB J,2005,19:425-427
    [39]Liang D, Bhatta S, Gerzanich V, et al.Cytotoxic edema:mechanisms of pathological cell swelling. Neurosurg Focus,2007,22(5):E2
    [40]Rash JE, Yasumura T, Hudson CS,et al.Direct immunogold labeling of aquaporin-4 in square arrays of astrocyte and ependymocyte plasma membranes in rat brain and spinal cord. Proc Natl Acad Sci USA,1998,95(20):11981-11986
    [41]Araque A. Astrocyte-neuron signaling in the brain-implications for disease. Curr Opin Investig Drug,2006 7:619-624.
    [42]Tait MJ, Saadoun S, Bell BA, et al. Water movements in the brain:role of aquaporins. Trends Neurosci,2008,31 (1):37-43
    [43]Reulen HJ, Graham R, Spatz M, et al.Role of pressure gradients and bulk flow in dynamics of vasogenic brain edema.J Neurosurg,1977,46(1):24-35
    [44]Marmarou A A review of progress in understanding the pathophysiology and treatment of brain edema. Neurosurg Focus,2007,22:E1
    [45]McClelland S Ⅲ, Long DM.Genesis of the use of corticosteroids in the treatment and prevention of brain edema. Neurosurgery,2008,62(4):965-968
    [46]Edwards P, Arango M, Balica L, et al. Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injury-outcomes at 6 months. Lancet,2005,365(9475):1957-1959
    [47]Hutchinson P, Timofeev I, Kirkpatrick P.Surgery for brain edema. Neurosurg Focus,2005,22(5):E14
    [48]Saadoun S, Papadopoulos MC, Davies DC, et al.Aquaporin-4 expression is increased in oedematous human brain tumours. J Neurol Neurosurg Psychiatry,2002,72:262-265
    [49]Warth A, Kroger S, Wolburg H. Redistribution of aquaporin-4 in human glioblastoma correlates with loss of agrin immunoreactivity from brain capillary basal laminae. Acta Neuropathol,2004,107(4):311-318
    [50]Papadopoulos MC, Verkman AS. Aquaporin-4 gene disruption in mice reduces brain swelling and mortality in pneumococcal meningitis. J Biol Chem,2005, 280:13906-13912
    [51]Badaut J, Brunet JF, Grollimund L, et al.Aquaporin 1 and aquaporin 4 expression in human brain after subarachnoid hemorrhage and in peritumoral tissue. Acta Neurochir Suppl,2003,86:495-498
    [52]Taniguchi M, Yamashi ta T, Kumura E,et al. Induction of aquaporin-4 water channel mRNA after focal cerebral ischemia in rats.Brain Res Mol Brain Res, 2002,78(1-2):131-137
    [53]Zeng HK, Wang QS, Deng YY, et al.Hypertonic saline ameliorates cerebral edema through downregulation of aquaporin-4 expression in the astrocytes.Neuroscience,2010,166(3):878-885
    [54]Ma T, Yang B, Gillespie A, et al. Generation and phenotype of a transgenic knockout mouse lacking the mercurial-insensitive water channel aquaporin-4. J Clin Invest,1997,100(5):957-962
    [55]Fan Y, Zhang J, Sun XL, et al. Sex-and region-specific alterations of basal amino acid and monoamine metabolism in the brain of aquaporin-4 knockout mice. J Neurosci Res,2005,82(4):458-464
    [56]Yang B, Zador Z, Verkman AS. Glial cell aquaporin-4 overexpression in transgenic mice accelerates cytotoxic brain swelling. J Biol Chem,2008,283:15280-15286
    [57]Amiry-Moghaddam M, Frydenlund DS, Ottersen OP.Anchoring of aquaporin-4 in brain:molecular mechanisms and implications for the physiology and pathophysiology of water transport.Neuroscience,2004,129(4):999-1010
    [58]Zeynalov E, Chen CH, Froehner SC, et al. The perivascular pool of aquaporin-4 mediates the effect of osmotherapy in postischemic cerebral edema. Crit Care Med,2008,36(9):2634-2640.
    [59]Amiry-Moghaddam M, Otsuka T, Hum PD, et al. An alpha-syntrophin-dependent pool of AQP4 in astroglial end-feet confers bidirectional water flow between blood and brain. Proc Natl Acad Sci U S A,2003,100:2106-2111
    [60]Papadopoulos MC, Verkman AS.Potential utility of aquaporin modulators for therapy of brain disorders. Prog Brain Res,2008,170:589-601

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