高渗盐对急性氨中毒大鼠效应的MR弥散及灌注成像研究
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摘要
第一部分高渗盐对急性氨中毒大鼠效应的MR弥散成像研究
     目的:研究急性氨中毒情况下大鼠MR弥散成像的表观弥散系数(ADC)的变化,以及高渗盐对此变化的影响。材料和方法:12只雄性SD大鼠随机分为二组,生理盐水对照组和高渗盐组,每组6只。12只大鼠分别腹腔注射醋酸铵5mmol/kg,浓度调整到每只注射量为3ml/kg:于用氨前,用氨后5min各自进行MR弥散成像,用于急性氨中毒况下大鼠的表观弥散系数(ADC)的变化研究。然后6只急性氨中毒大鼠通过股静脉滴注23.4%高渗盐溶液,6ml/kg,15min滴完;另6只急性氨中毒大鼠通过股静脉滴注生理盐水作为对照;之后马上进行MR弥散成像。原始图象运用GE Functiontool软件处理,分别选定双侧尾壳核、运动皮层、感觉皮层、丘及小实质为兴趣区(ROI),获得兴趣区(ROI)的表观弥散系数(ADC)平均值。结果:在所选10个兴趣区中,用氨前后双侧尾壳核ADC值降低达到统计学有意义;滴注23.4%高渗盐溶液后所有选定兴趣区的ADC值均较对照组高,然而并未达到统计学有意义。
     结论:急性氨中毒导致双侧尾壳核细胞毒性水肿;高渗盐溶液引起几乎所有ROI的ADC值升高,但均未达到统计学意义,是否与测量时点过早有关,尚需进一步研究。
     第二部分急性氨中毒大鼠MR灌注成像研究
     目的:研究急性氨中毒情况下大鼠的MR灌注成像的NEI(negative enhancedintegral,负性增强积分),MSD(maximum slope of decrease,最大下降斜率)和MTT(mean transit time,平均通过时间)值的变化,探讨急性氨中毒大鼠的灌注变化规律。材料和方法:12只大鼠随机(数字表法)分为空白对照组和氨中毒组,每组6只。氨中毒组6只大鼠均以腹腔注射醋酸铵的方法造成急性氨中毒。大鼠模型制备后5min行MR扫描。原始图像传送至工作站(AdvantageWorkstation AW4.0-05,GE公司),采用Functiontool灌注软件处理,分别获得NEI、MSD和MTT参数图,选择尾壳核(CPu)、运动皮层(MCx),感觉皮层(SCx),丘(Tha)及小(Cb)实质为兴趣区(ROI);分别测量上述部位的NEI、MSD和MTT值,然后取双侧小(Cb)实质均值并分别计算上述左侧或右侧兴趣区(ROI)与之的比值,得到相对NEI、MSD和MTT(rNEI、rMSD及rMTT),两组进行比较。结果:氨中毒后所选各个区rMTT值均较对照组缩短,并且达到统计学意义;rNEI及rMSD与对照组相比没有明显差异。结论:急性氨中毒导致大鼠灌注血流增加,提示可能存在充血改变。磁共振灌注成像可以反映急性氨中毒大鼠微循环的变化。
     第三部分高渗盐对急性氨中毒大鼠效应的MR灌注成像研究
     目的:研究高渗盐对急性氨中毒情况下大鼠的MR灌注成像的NEI(negative enhanced integral,负性增强积分),MSD(maximum slope ofdecrease,最大下降斜率)和MTT(mean transit time,平均通过时间)值的影响,进而揭示高渗盐对急性氨中毒大鼠灌注的影响。材料和方法:24只大鼠随机(数字表法)分为生理盐水组、高渗盐组、氨+生理盐水组、氨+高渗盐组,每组6只。其中氨+生理盐水组、氨+高渗盐组的12只大鼠均以腹腔注射醋酸铵造成急性氨中毒;然后按照预先分组6只急性氨中毒大鼠通过股静脉滴注23.4%高渗盐溶液;另6只急性氨中毒大鼠通过股静脉滴注相同剂量生理盐水作为对照。另两组生理盐水组、高渗盐组只通过股静脉滴注23.4%高渗盐溶液或生理盐水,15min滴完,作为对照:之后马上进行MR成像。原始图像传送至工作站(Advantage Workstation AW4.0-05,GE公司),采用Functiontool灌注软件处理,分别获得NEI、MSD(maximum slode of decrease,最大下降斜率,相当于局部血流流入速度)和MTT参数图,选取尾壳核(CPu)、运动皮层(MCx),感觉皮层(SCx),丘(Tha)及小(Cb)实质为兴趣区(ROI),分别测得双侧上述ROI的NEI、MSD、MTT值,然后取双侧小(Cb)实质均值并分别计算上述左侧或右侧兴趣区(ROI)与之的比值,得到相对NEI、MSD和MTT(rNEI、rMSD及rMTT),然后四组进行比较。结果:左侧尾壳核区的rNEI值氨+高渗盐组及高渗盐组低于氨+生理盐水组,具有统计学意义;右侧尾壳核区的rNEI值氨+生理盐水组较其他三组均高,且具有统计学意义;而其他各区rNEI值比较没有明显差异。各组rMTT及rMSD值比较均无明显差异。
     结论:大鼠急性氨中毒尾壳核区存在充血变化,高渗盐溶液输注后可引起尾壳核区的rNEI值降低,表明高渗盐溶液可缓解大鼠急性氨中毒后尾壳核区高灌注状态,所以高渗盐可以缓解急性氨中毒大鼠高灌注,有利于水肿缓解。
PartⅠ:Effect of hypertonic saline on rats with acute ammonia intoxication:a study utilizing diffusion-weighted magnetic resonance imaging
     Purpose:To investigate the value of Apparent diffusion coefficient in rats with acute ammonia intoxication before and after using hypertonic saline.Materials and Methods:twelve male SD rats were randomly divided into two groups.12 rats were performed MR diffusion-weighted imaging before and after they were injected intraperitoneally with ammonium acetate;and then 6 rats were injected by femoral vein with hypertonic saline and the other 6 control rats were injected by femoral vein with saline.After 15min MR imaging were performed.Apparent diffusion coefficient(ADC)topographical maps were archived by the Workstation(AW4.0-05,GE).The values of ADC of the right or left sensory cortex,caudate-putamen,thalamus, cerebellar hemisphere and the motor cortex were measured.Results:We measured ADC in 10 brain regions,ADC decrease only in bilaeral caudate-putamen.The using hypertonic saline dose not influence the values of ADC in 15min.Conclusion:The values of ADC decrease in bilaeral caudate-putamen suggested ammonia induced cytotoxic edema in rats with acute ammonia intoxication.Hypertonic saline dose not influence the values of ADC in short time period.
     PartⅡ:Study of rats with acute ammonia intoxication with magnetic resonance perfusion imaging
     Purpose:To investigate the change of the value of NEI (negative enhanced integral),MSD(maximum slope of decrease) and MTT (mean transit time) in rats with acute ammonia intoxication.Materials and Methods:twelve male SD rats were randomly divided into twogroups.6 rats were performed MR perfusion-weighted imaging after they were injected intraperitoneally with ammonium acetate;and then the other 6 control rats were performed MR perfusion-weighted imaging.NEI、MSD and MTT topographical maps were archived by the Workstation(AW4.0-05,GE). The values of NEI、MSD and MTT of the right or left sensory cortex, caudate-putamen,thalamus,cerehellar hemisphere and the motor cortex were measured.Then take mean NEI,MSD and MTT of two-sides of cerebellar hemisphere ROIs in every rat,the relative NEI,MSD and MTT(rNEI、rMTT and rMSD) were calculated as ratios to the averged left and right cerebellar values.Take the ratios of two groups into statistical analysis.Results:relative MTT prolonged in everv ROIs after poisoning, had statistical significance(P<0.05),which compared with pre-poisoning;relative NEI and MSD of poisoned rats compared with pre-poisoning have no significant differences.Conclusion:Rats with acute ammonia intoxication can be obvered cerebral hyperemia in all ROIs. MR perfusion weighted imaging can reflect changes of the microcirculation of the poisoned rats' brain,which suggest that brain microcirculation severe disturbance is possibly one of the causes which aggravate brain injury and induce delayed encephalopathy.
     PartⅢ:Effect of hypertonic saline on rats with acute ammonia intoxication:a study utilizing perfusion - weighted magnetic resonance imaging
     Purpose:To apply MR perfusion weighted imaging to reflect the changes of the perfusion of rat in acute ammonia poisoning before and after using hypertonic saline.Materials and Methods:24 male SD rats were randomly divided into four groups,ammonia plus hypertonic saline,ammonia plus saline,saline and hypertonic saline.12 rats were injected intraperitoneally with ammonium acetate;and then 6 rats were injected by femoral vein with hypertonie saline and the other 6 control rats were injected by femoral vein with saline,after 15min MR perfusion-weighted imaging were performed.the other group were injected by femoral vein with hypertonic saline and saline,after 15min MR perfusion-weighted imaging were performed too.NEI、MSD and MTT topographical maps were archived by the Workstation(AW4.0-05,GE).The values of NEI、MSD and MTT of the right or left sensory cortex, caudate-putamen,thalamus,cerebellar hemisphere and the motor cortex were measured.Then take mean NEI,MSD and MTT of two-sides of cerebellar hemisphere ROIs in every rat,the relative NEI,MSD and MTT(rNEI、rMTT and rMSD) were calculated as ratios to the averged left and right cerebellar values.Take the ratios of four groups into statistical analysis.Results:Relative MTT and MSD had no remarkable changes in four groups.Relative NEI(rNEI) decreased in group of ammonia plus hypertonic saline in the caudate-putamen ROIs,which compared with that of ammonia plus saline;had statistical significance(P<0.05). The values of relative NEI(rNEI) in groups of saline and hypertonic saline are low than that of in group of ammonia plus hypertonic saline in the caudate-putamen ROIs,had statistical significance(P<0.05).Conclusion:The values of relative NEI decrease in group of ammonia plus hypertonic saline in eaudate-putamen suggested perfusion cut down.So hypertonic saline can relieve brain hyperemia in rats with acute ammonia intoxication.
引文
[1].何杰,刘怀军,黄勃源,等。正常成人组织弥散成像的定量研究。河北医科大学学报,2006,4:267-270
    [2].叶瑞心,张卫东,梁碧玲.B值强度和数目对组织ADC值测定的影响.影像诊断与介入放射学,2004,1:3-6
    [3]Miller KL,Bult DP,Devlin H,et al..Evidence for a vascular contribution to diffusion FMRI at high b value.Proc Natl Acad Sci,2007,104(52):20967-20972
    [4]Cauli O,Lopez-Larrubia P,Rodrigues TB,et al.Magnetic resonance analysis of the effects of acute ammonia intoxication on rat brain.Role of NMDA receptors.J Neurochem,2007,103:1334-1343
    [5]廖承德,韩丹.高氨血症与急性肝性病.云南医药,2005,26(2):166-168
    [6]Pedersen HR,Ring-Larsen H,Olsen NV et al.Hyperammonemia acts synergistically with lipopolysaccharide in inducing changes in cerebral hemodynamics in rats anaesthetised with pentobarbital.J Hepatol,2007,47:245-252
    [7]AhI B,Karin Weissenborn K,van den Hoff J,et al.Regional differences in cerebral blood flow and cerebral ammonia metabolism in patients with cirrhosis;Hepatology,2004,40(1):73-79
    [8]Ranjan P,Mishra AM,Kale R,et al.Cytotoxic edema is responsible for raised intracranial pressure in fulminant hepatic failure:in vivo demonstration using diffusion-weighted MRI in human subjects.Metab Brain Dis,2005,20(3):181-192
    [9]Norenberg.Astroglial dysfunction in hepatic encephalopathy.Metab Brain Dis.1998,13:319-335
    [10]Rovira A,Cordoba J,Raguer N,et al.Magnetic resonance imaging measurement of brain edema in patients with liver disease:Resolution after liver transplantation.Curr Opin Neurol,2002,15(6):731-737
    [11]Ogden AT,Mayer SA,Connolly ES,et al.Hyperosmolar agents in neurosurgical practice:the evolving role of hypertonic saline.Neurosurgery,2005,57(2):207-215
    [12]Mirski MA,Denchev ID,Schnitzer SM,et al.Comparison between hypertonic saline and mannitol in the reduction of elevated intracranial p ressure in a rodent model of acute cerebral injury.J Neurosurg Anesthesiol,2000,12(4):334-344.
    [13]White H,Cook D,Venkatesh B.The use of hypertonic saline for treating intracranial hypertension after traumatic brain injury. Anesth Analg, 2006, 102 (6): 1836-1846
    
    [14] Toung TJ, Nyquist P, Mirski MA. Effect of hypertonic saline concentration on cerebral and visceral organ water in an uninjured rodent model. Crit Care Med.2008, 36(1):256-261
    
    [15] Strauss G, Hansen BA, Knudsen GM,et al. Hyperventilation restores cerebral blood flow autoregulation in patients with acute liver failure.J Hepatol, 1998, 28(2): 199-203
    
    [16] Feltracco P, Serra E, Barbieri S. Cerebral blood flow in fulminant hepatitis. transplantation proceedings, 2006,38, 786-788
    
    [17] Jalan R, Olde Damink SW, Deutz NE, et al. Restoration of cerebral blood flow autoregulation and reactivity to CO2 in acute liver failure by moderate hypothermia. Hepatology 2001,34:50-4.
    
    [18] Clemmesen JO, Hansen BA, Larsen FS. Indomethacin normalizes intracranial pressure in acute liver failure: a twenty-three-year-old woman treated with indomethacin. Hepatology 1997;26:1423-5.
    
    [19] Ede RJ, Williams R. Hepatic encephalopathy and cerebral edema. Semin Liv Dis 1986;6:107-118.
    
    [20 ] Blei AT . Cerebral edema and intracranial hypertension in acute liver failure: distinct aspects of the same problem. Hepatology, 1991, 13:376-379
    [21] Ben Abraham R, Szold O, Merhav H,et al.Rapid resolution of brain edema and improved cerebral perfusion pressure following the molecular adsorbent recycling system in acute liver failure patients. Transplantation proceedings, 2001, 33:2897-2899
    
    [22] Strauss GI, H(?)gh P, M(?)ller K, et al.Regional cerebral blood flow during mechanical hyperventilation in patients with fulminant hepatic failure. Hepatology 1999,30:1368-1373.
    
    [23] Yang ST , Chang HH. Nitric oxide of neuronal origin mediates NMDA - induced cerebral hyperemia in rats ._Neuroreport,1998,9(3):415- 418.
    [24 ] Rao VL , Audet RM. Increased neuronal nitric oxide synthese expression in brain following portacaval anastomosis . Brain Res , 1997 , 765 : 169-172.
    [25] Larsen FS, Wendon J. Brain edema in liver failure: Basic physiologic principles and management. J Liver Transpl. 2002, 8:983-989.
    [26] Norenberg,M.D. Astroglial dysfunction in hepatic encephalopathy. Metab. Brain Dis.1998,13:319-335.
    [27]Rovira A,Cordoba J,Raguer N,et,al.Magnetic resonance imaging measurement of brain edema in patients with liver disease:Resolution after liver transplantation.Curr Opin Neurol.2002,15:731-737.
    [28]Willard-Mack CL,Koehler RC,HirataT,et,al.Inhibition of glutamine synthase reduces ammonia-induced astrocyte swelling in rats.Neuroscience.1996,71:589-599.
    [29]Clemmensen JO,Larsen FS,Kondrup J,et,al.Cerebral herniation in patients with acute liver failure is correlated with arterial ammonia concentration.Hepatology,1999,29:648-63.
    [30]Rose C,Michalak A,Pannunzio M,et,al.Mild hypothermia delays the onset of coma and prevents brain edema and extracellular brain glutamate accumulation in rats with acute liver failure.Hepatology.2000,31:872-877.
    [31]Iwasa M,Matsumura K,Nakagawa Y,et al.Evaluation of cingulate gyrus blood flow in patients with liver cirrhosis.Matebol Brain Dis,2005,20(1):7-17
    [32]Schaefer PW,Grant PE,Gonzalez RG.Diffusion-weighted MR imaging of the brain.Radiology,2000,217:331-345.
    [33]Chan R,Erbay S,Oljeski S,et,al.Hypoglycemia and diffusion-weighted imaging.J Comput Assist Tomogr.2003,27:420-423.
    [34]Tominaga S,Watanabe A,Tsuji T.Synergistic effect of bile acid,endotoxin,and ammonia on brain edema.Metab.Brain Dis.1991,6:93-105.
    [35]李涛,马林,周卫华等.亚临床期肝性病MRI及血流灌注成像的研究.临床放射学杂志,2006,25(7):602-605
    [36]Takahashi H,Koehler RC,Brusilow SW,Traystman RJ.Inhibition of brain glutamine accumulation prevents cerebral edema in hyperammonemic rats.Am J Physiol,1991,261:H825-H829.
    [37]Masters S,Gottstein J,Blei AT.Cerebral blood flow and the development of ammonia-induced brain edema in rats after portacaval anastomosis.Hepatology,1999,30:878-880.
    [38]Blei AT,Larsen FS.Pathophysiology of cerebral edema in fulminant hepatic failure.J Hepatol 1999;31:771-776.
    [39]Canalese J,Gimson AE,Davis C,Melton PJ,Davis M,Williams R.Controlled trial of dexamethasone and mannitol for the cerebral oedema of fulminant hepatic failure.Gut 1982;23:625-629.
    [40]Cordoba J,Gottstein J,Blei AT.Chronic hyponatremia exacerbates ammonia-induced brain edema in rats after portacaval anastomosis. J Hepatol, 1998;29:589-594.
    
    [41]Larsen FS, Ejlersen E, Hansen BA, et al. Functional loss of cerebral blood flow autoregulation in patients with fulminant hepatic failure. J Hepatol,1995, 23:212-7
    
    [42] Larsen FS, Ejlersen E, Strauss G, et al. Cerebrovascular metabolic autoregulation is impaired during liver transplantation. Transplantation, 1999, 68: 1472-6
    
    [43]Hirata T, Koehler RC, Brusilow SW, et al. Preservation of cerebral blood flow responses to hypoxia and arterial pressure alterations in hyperammonemic rats. J Cereb Blood Flow Metab,1995, 15:835-44
    
    [44] Jalan R, Steven WM, Damink O, et al.Oral Amino Acid Load Mimicking Hemoglobin Results in Reduced Regional Cerebral Perfusion and Deterioration in Memory Tests in Patients with Cirrhosis of the Liver.Metabolic Brain Disease, 2003, 18(1):37-49
    
    [45] Larsen FS , Gottstein J, Andreas T, Cerebral hyperemia and nitric oxide synthase in rats with ammonia-induced brain edema J Hepatol, 2001, 34:548-554
    
    [46] Larsen FS, Strauss G, Knudsen GM, et al. Cerebral perfusion, arterial pressure and cardiac output in patients with acute liver failure. Crit Care Med, 2000,18:996-1001.
    
    [47] Sugimoto H, Koehler RC, Wilson DA, et al.Methionine sulfoximine, a glutamine synthetase inhibitor, attenuates increased extracellular potassium activity during acute hyperammonemia. Cereb Blood Flow Metab 1997,17:44-49.
    
    [48] Clemmesen JO, Hansen BA, Larsen FS. Indomethacin normalizes intracranial pressure in acute liver failure: a twenty-three-year-old woman treated with indomethacin. Hepatology, 1997,26:1423±1425.
    
    [49] Cordoba J, Crespin J, Gottstein J, Blei AT. Mild hypothermia modifies ammonia-induced brain edema in rats after portacaval anastomosis. Gastroenterology, 1999,116:686-693.
    
    [50] Masters S, Gottstein J, Blei AT. Cerebral blood flow and the development of ammonia-induced brain edema in rats after portacaval anastomosis. Hepatology, 1999,30:878-880.
    
    [51] Rao VL, Audet RM, Butterworth RF. Increased neuronal nitric oxide synthase expression in brain following portacaval anastomosis. Brain Res, 1997,765:169-172.
    [52] Iadecola C, Pelligrino DA, Moskowitz MA, et al. Nitric oxide inhibition and cerebrovascular regulation. J Cereb Blood Flow Metab, 1994,14:175-192.
    [53] Aggarwal S, Kramer D, Yonas H, et al.Cerebral hemodynamic and metabolic changes in fulminant hepatic failure: a retrospective study. Hepatology,1994,19:80-87.
    
    [54] Wendon JA, Harrison PM, Keays R, Williams R. Cerebral blood flow and metabolism in fulminant liver failure. Hepatology, 1994,19:1407-1413.
    
    [55] Larsen FS, Pott F, Hansen BA, Knudsen GM, Ejlersen E, ClemmesenJO, et al. Transcranial doppler sonography may predict brain death in patients with fulminant hepatic failure. Transplant Proc, 1995,6:3510-3511.
    
    [56] Filho JA, Machado MA, Nani RS. Hypertonic saline solution increases cerebral perfusion pressure during clinical orthotopic liver transplantation for fulminant hepatic failure: Preliminary results clinics, 2006,61(3):231-8
    
    [57] Murphy N, Auzinger G, Bernel W, et al.The Effect of Hypertonic Sodium Chloride on Intracranial Pressure in Patients With Acute Liver Failure. Hepatology 2004;39:464-470.
    
    [58] Kato M, Hughes RD, Keays RT, et al. Electron microscopic study of brain capillaries in cerebral edema from fulminant hepatic failure. Hepatology, 1992,15:1060 -1066.
    
    [59] Gove CD, Hughes RD, Ede RJ,et al. Regional cerebral edema and chloride space in galactosamine-induced liver failure in rats. Hepatology,1997,25:295-301.
    
    [60]Shackford SR, Schmoker JD, Zhuang J. The effect of hypertonic resuscitation on pial arteriolar tone after brain injury and shock. J Trauma, 1994,37:899 -908.
    
    [61] Doyle JA, Davis DP, Hoyt DB. The use of hypertonic saline in the treatment of traumatic brain injury. J Trauma, 2001, 50 (2) : 367 -383
    
    [62]Nakayama S, Kramer GC, Carlsen RC, et al. Infusion of hypertonic saline to bled rats: membrane potentials and fluid shifts. J Surg Res, 1985,38:180 -186.
    
    [63]Doyle J, Davis D, Hoyt D. The use of hypertonic saline in the treatment of traumatic brain injury. J Trauma Inj Infect Crit Care, 2001,2:367-83.
    
    [64] Pascual JM, Solivera J, Prieto R, et al. Time course of early metabolic changes following diffuse traumatic brain injury in rats as detected by(l) H NMR spectroscopy. J Neurotrauma, 2007, 24 (6) : 944 -959.
    
    [65]Boulard G,Marguinaud E, SesayM. Osmotic cerebral edema: the role of plasma osmolarity and blood brain barrier. Ann Fr Anesth Reanim, 2003, 22 (3) : 215 - 219.
    
    [66] Muizelaar JP, Wei EP, Kontos HA, et al. Mannitol causes compensatory cerebral vasoconstriction and vasodilation in response to blood viscosity changes. J Neurosurg, 1983,59:822-8.
    
    [67] Hudak ML, Jones Jr MD, Popel AS, et al.Hemodilution causes size-dependent constriction of pial arterioles in the cat. Am J Physiol, 1989,257:H912-7.
    
    [68] Burke AM, Quest DO, Chien S, et al. The effects of mannitol on blood viscosity. J Neurosurg, 1981,55:550-3
    
    [69] Brain Trauma Foundation, American Association of Neurological Surgeons, Joint Section on Neurotrauma and Critical Care. Guidelines for the management of severe head injury. J Neurotrauma, 2000,6-7:449-627.
    
    [70] Khanna S,DavisD, Peterson B, et al. Use of hypertonic saline in the treatment of severe refractory posttraumatic intracranial hypertensionin pediatric traumatic brain injury. Crit CareMed, 2000, 28 (4) :1144 - 1151.
    
    [71] Schwarz S, Georgiadis D, Aschoff A, et al. Effects of hypertonic (10%) saline in patients with raised intracranial pressure afterstroke. Stroke, 2002, 33 (1) : 136-140.
    
    [72] Huang SJ, Chang L, Han YY, et al. Efficacy and safety of hypertonic saline solutions in the treatment of severe head injury. Surg Neurol, 2006, 65 (6): 539 - 546.
    
    [73] ELena K,Marta L, CarmineM. Glutamine synthetase activity and glutamine content in brain: modulation by NMDA recep tors and nitric oxide. Neurochemist, 2003, 43 (4 - 5) : 493 - 499.
    
    [74] Small DL,Morley P, Buchan AM. Biology of ischemsic cerebral cell death. Prog Cardiovasc Dis, 1999, 42 (3): 185 - 207.
    
    [75]Hindfelt B , Siesjo¨ BK. Cerebral effects of acute ammonia intoxication. Ⅱ. The effect upon energy metabolism. Scand. J. Clin.Lab. Invest.1971, 28, 365-374.
    
    [76] Qureshi AI, Suarez JI. Use of hypertonic saline solutions in treatment of cerebral edema and intracranial hypertension. Critical Care Medicine, 2000, 28: 3301-3313.
    [1] Ferenci P, Lockwood A, Mullen K,et al. Hepatic encephalopathy-Definition, Nomenclature,Diagnosis, and Quantification: Final report of the Working Party at the 11th World Congresses of Gastroenterology.Hepatology. 2002;35:716-721
    
    [2] Ranjan P, Mishra AM, Kale R, et al. Cytotoxic Edema Is Responsible for Raised Intracranial Pressure in Fulminant Hepatic Failure:In Vivo Demonstration Using Diffusion-Weighted MRI in Human Subjects. Metabol Brain Dis. 2005, 20(3): 181-193
    
    [3] Arnold SM, Eis T,Spreer J,et al.Acute hepatic encephalopathy with diffuse cortical lesions.Neuroradiology. 2001,43:551-554
    
    [4] Rovira A, Cordoba J, Raguer N, et al. Magnetic resonance imaging measurement of brain edema in patients with liver disease: resolution after transplantation. Curr Opin Neurol.2003,15(6):731-7
    
    [5] Aggarwal A, Vaidya S, Shah S, et al. Reversible Parkinsonism and T1W Pallidal Hyperintensities in Acute Liver Failure. Mov Disord. 2006,21(11):1986-1989
    
    [6] Skehanl S, Norris S, Hegarty J, et al. Brain MRI changes in chronic liver disease. Eur. Radiol. 1997, 7: 905-909
    
    [7] Uchino A, Hasuo K, Matsumoto S, et al.Cerebral MR imaging in patients with primary biliary cirrhosis .Nippon Igaku Hoshasen Gakkai Zasshi.1993, 53(2): 145-9
    
    [8] Krieger S, Jauss M, Jansen O, et al.MRI findings in chronic hepatic encephalopathy depend on portosystemic shunt:results of a controlled respective clinical investigation. J Hepatol. 1997,21: 121-126
    
    [9] Matsusue E, Kinoshita T, Ohama E, et al..Cerebral Cortical and White Matter Lesions in Chronic Hepatic Encephalopathy:MR-Pathologic Correlations. AJNR Am J Neuroradiol.2005, 26:347-351
    
    [10] Rovira A, Cordoba J, Sanpedro F. Normalization of T2 signal abnormalities in hemispheric white matter with liver transplant. Neurology. 2002,59:335-341
    
    [11] Grover VP, Dresner MA, Forton DM,et al. Current and future applications of magnetic resonance imaging and spectroscopy of the brain in hepatic encephalopathy World J Gastroenterol 2006; 12(19): 2969-2978
    
    [12] Miese F, Kircheis G, Wittsack HJ,et al. ~1H-MR Spectroscopy, Magnetization Transfer, and Diffusion-Weighted Imaging in Alcoholic and Nonalcoholic Patients with Cirrhosis with Hepatic Encephalopathy. AJNR Am J Neuroradiol. 2006, 27:1019-26,
    
    [13] Mechtcheriakov S, Schocke M, Kugener A, et al. Chemical shift magnetic resonance spectroscopy of cingulate grey matter in patients with minimal hepatic encephalopathy. Neuroradiology .2005,47: 27-34
    
    [14] Lodi R, Tonon C, Stracciari A,et al. Diffusion MRI shows increased water apparent diffusion coefficient in the brains of cirrhotics .Neurology. 2004,62:762-766
    
    [15] Nolte W, Wiltfang J, Christian CG, et al. Bright basal ganglia in T1-weighted magnetic resonance images are frequent in patients with portal vein thrombosis without liver cirrhosis and not suggestive of hepatic encephalopathy J Hepatol, 1998; 29: 443-449
    
    [16] Crespin J, Nemcek A, Rehkemper G,et al. Intrahepatic Portal-Hepatic Venous Anastomosis: A Portal-Systemic Shunt With Neurological Repercussions. Am J Gastroenterol.2000,95( 6): 1568-1571
    
    [17] Patel N, White S, Dhanjal NS, et al. Changes in brain size in hepatic encephalopathy: a coregistered MRI study.Metabolic Brain Disease. 2004,19:431-445
    
    [18] Gupta RK, Dhiman RK. Magneitc resonance imaging and spectroscopy in hepatic encephalopathy. Indian J Gastmentetalqf.2003, 22(12): 45-49
    
    [19] McConnell, JR, Antonson DL, Ong CS, et al. Proton spectroscopy of brain glutamine in acute liver failure. Hepatology.1995, 22(1): 69-74
    
    [20] Gupta RK, Saraswat VA, Poptani H, et al.Magnetic resonance imaging and localized in vivo proton spectroscopy in patients with fulminant hepatic failure. Am.J. Gastroenterol.1993, 88:670-674.
    
    [21] Rovira A, Grive E, Pedraza S, et al. Magnetization transfer ratio values and proton MR spectroscopy of normal-appearing cerebral white matter in patients with liver cirrhosis. AJNR Am J Neuroradiol.2001,22(6): 1137-42
    
    [22] Shah NJ, Neeb H, Zaitsev M, et al.Quantitative T1 Mapping of Hepatic Encephalopathy Using Magnetic Resonance Imaging. Hepatology, 2003,38(5):1219-1226
    
    [23] Fukuzawa T , Matsutani S, Maruyama H ,et al.Magnetic resonance images of the globus pallidus in patients with idiopathic portal hypertension: A quantitative analysis of the relationship between signal intensity and the grade of portosystemic shunt. J Gastroenterol Hepatol. 2006,21(5):902-907
    
    [24] Krieger D, Krieger S, Jansen O, et al. Manganese and chronic hepatic encephalopathy. Lancet ,1995,346: 270-274
    
    [25] Maeda H, Sato M, Yoshikawa A,et al. Brain MR imaging in patients with hepatic cirrhosis: relationship between high intensity signal in basal ganglia on T1-weighted images and elemental concentrations in brain .Neuroradiology ,1997, 39: 546-550
    
    [26] Hauser RA, Zesiewicz TA, Rosemurgy AS,et al. Manganese intoxication and chronic liver failure.Ann Neurol ,1994,36: 871-875.
    
    [27] Ejima A, Imamura T, Nakamura S, et al. Manganese intoxication during total parenteral nutrition. Lancet ,1992,339: 426.
    
    [28] Mirowitz SA, Westrich TJ. Basal ganglial signal intensity alterations: reversal after discontinuation of parenteral manganese administration. Radiology ,1992,185: 535-536.
    
    [29]Martin M, Zajko AB. Orons PD, et al. Trdnsjugular intrahepatic portosystemic shunt in the management of variceal bleeding: indications and clinical results. Surgery, 1993, 114:719-727.
    
    [30] Krieger S, Jauss M, Jansen O, et al. MRI findings in chronic hepatic encephalopathy depend on portosystemic shunt:results of a controlled rospective clinical investigation. J Hepatol, 1991, 21: 121-126
    
    [31]Pal PK, Samii A, Calne DB. Manganese neurotoxicity: A review of clinical features, imaging and pathology. Neurotoxicology ,1999,20, 227-238
    
    [32] Dorman DC, Struve MF, Wong BA, et al.Correlation of Brain Magnetic Resonance Imaging Changes with Pallidal Manganese Concentrations in Rhesus Monkeys Following Subchronic Manganese Inhalation.Toxico sci.2006,92 (1) :219-227
    
    [33] Patel N, White S, Dhanjal NS, et al. Changes in brain size in hepatic encephalopathy: a coregistered MRI study.Metabolic Brain Disease. 2004,19:431-445
    
    [34]. Cordoba J, Alonso J, Rovira A, et al. The development of low-grade cerebral edema in cirrhosis is supported by the evolution of (1)H-magnetic resonance abnormalities after liver transplantation. J Hepatol 2001;35:598-604.
    [35].Lucchini R, Albini E, Placidi D, Gasparotti R, Pigozzi MG, Montani G,Alessio L. Brain magnetic resonance imaging and manganese exposure.Neurotoxicology ,2000,21:769-775.
    
    [36]Norenberg M.D. Astroglial dysfunction in hepatic encephalopathy. Metab. Brain Dis. 1998,13:319-335.
    
    [37]Rovira A, Cordoba J, Raguer N, et al. Magnetic resonance imaging measurement of brain edema in patients with liver disease: Resolution after liver transplantation. Curr. Opin. Neurol.2002, 15:731-737.
    
    [38]Willard-Mack CL, Koehler RC, Hirata T, et al. Inhibition of glutamine synthase reduces ammonia-induced astrocyte swelling in rats. Neuroscience, 1996,71:589-599.
    [39]Cordoba J, Gottstein J, Blei AT. Glutamine, myo-inositol, and organic brain osmolytes after portacaval anastomosis in the rat: Implications for ammonia-induced brain edema. Hepatology,1996, 24:919-923.
    
    [40] Taylor-Robinson SD, Buckley C, Changani KK,et al.Cerebral proton and phosphorus-31 magnetic resonance spectroscopy in patients with subclinical hepatic encephalopathy. Liver, 1999,19:389-398.
    
    [41]7. Bluml S, Moreno-Torres A, Ross BD. [1-13C]glucose MRS in chronic hepatic encephalopathy in man. Magn Reson Med, 2001,45:981-993.
    
    [42] Willard-Mack CL, Koehler RC, Hirata T, et al. Inhibition of glutamine synthetase reduces ammonia-induced astrocyte swelling in rat. Neuroscience ,1996;71:589-599.
    
    [43] Laubenberger J, Ha¨ussinger D, Bayer S, et al.Proton magnetic resonance spectroscopic studies of the brain in symptomatic and asymptomatic patients with liver cirrhosis. Gastroenterology, 1997,112:1610-1616.
    
    [44] Kale RA, Gupta RK, Saraswat VA,et al.Demonstration of Interstitial Cerebral Edema With Diffusion Tensor MR Imaging in Type C Hepatic .Encephalopathy .Hepatology, 2006,43(4):698-706
    
    [45] Iwasa M, Matsumura K, Nakagawa Y, et al.Evaluation of Cingulate Gyrus Blood Flow in Patients With Liver Cirrhosis.Metabolic Brain Disease,2005,20 (1) :7-17
    [46] ATI B,Weissenbom K,van den Hof J, et al. Regional differences in cerebrl blood flow and cerebral al,ulnonia metabolism in patients with cirrhosis. Hepatology,2004, 40(1): 73-79

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