Hyperbaric oxygen induces rapid protection against focal cerebral ischemia

BACKGROUND AND PURPOSE: The timing and mechanisms of protection by hyperbaric oxygen (HBO) in cerebral ischemia have only been partially elucidated. We monitored the early in vivo effects of HBO after 2 h transient focal ischemia using repetitive MRI. METHODS: Wistar rats underwent filament occlusion of the middle cerebral artery (MCAO). 40 min after MCAO, rats were placed in a HBO chamber and breathed either 100% O(2) at 3.0 atmospheres absolute (ata; n = 24) or at 1.0 ata (control; n = 24) for 1 h. Diffusion, perfusion and T2-weighted MR-images were obtained after 15 min and 3, 6 and 24 h of reperfusion. In 6 axial MR slices, volume of abnormal diffusion and T2w signals were measured in the ischemic hemisphere. Furthermore, hemispheric mean apparent diffusion coefficient- (ADC) and T2 values were calculated for statistical analysis. RESULTS: HBO significantly reduced volume of abnormal DWI signal beginning immediately after reperfusion (control: 92 +/- 28 mm(3); HBO: 64 +/- 17) and lesion size on T2w (control: 375 +/- 91 mm(3); HBO: 225 +/- 39) after 24 h. Correspondingly, mean ADC levels were lower and T2 values higher in the ischemic hemisphere in the control group. HBO reduced histological infarct size at 24 h. CONCLUSION: High-dose intraischemic HBO therapy has an immediate protective on the brain which is superior to normobaric oxygen.     

USPIO增强核磁共振活体内监测局部脑缺血再灌注损伤的炎症反应

目的 探讨超微超顺磁性氧化铁粒子(USPIO)增强磁共振(MR)活体监测局部脑缺血再灌注损伤炎症反应的可行性.方法 40只雄性SD大鼠按照随机数字表法分为5组:氯化三苯基四氮唑(TTC)染色组(n=4)、假手术组(n=6)、缺血再灌注24 h组(n=10)、缺血再灌注48 h(n=10)和缺血再灌注72h组(n=10).局部脑缺血再灌注模型制作成功后经大鼠尾静脉注射USPIO,分别于再灌注24 h、48 h、72 h行MR扫描.成像后分别于相应的时间点处死大鼠,取脑组织冰冻切片行HE染色观察细胞死亡.普鲁士蓝染色观察铁粒,CD68免疫组织化学染色和荧光标记观察巨噬细胞(活化的小胶质细胞).结果 成功的模型可以在T2WI上看到高信号的水肿区,USPIO在T1WI上呈正性强化,T2WI上呈负性增强;24hT1WI增强信号缺血侧/对侧比值为1.60±0.28,稍高于48h和72 h,48 h T2WI增强信号缺血侧/对侧比值为0.92±0.17,稍高于24 h和72 h,对照组中信号无类似变化;各时间点T1WI缺血侧增强效应均明显高于T2WI,差异有统计学意义(P<0.05).普鲁士蓝染色证实梗死灶周边及坏死灶内可见铁粒子沉积.CD68免疫组化染色显示小胶质细胞增生活跃.结论 应用USPIO这种相对细胞特异的MR对比剂,可以活体动态观察局部脑缺血再灌注损伤的炎症反应变化.     

Spectacular shrinking deficit: insights from multimodal magnetic resonance imaging after embolic middle cerebral artery occlusion in Sprague-Dawley rats.

Almost no data is available on the serial changes in the brain after spectacular shrinking deficit (SSD) that may help understand this relatively rare clinical phenomenon. Quantitative diffusion-(DWI), perfusion-(PWI), T(1)-(T1WI), T(2)-weighted (T2WI), and functional magnetic resonance imaging (fMRI) were performed before, during, and up to 7 days after embolic middle cerebral artery occlusion (eMCAO) in male Sprague-Dawley rats (n=9). Region of interest (ROI) analysis was used to evaluate structural and functional MR signal changes within three ROIs defined by the apparent diffusion coefficient (ADC), cerebral blood flow (CBF) signatures, and final tissue viability. DWI, PWI, and T2WI lesion volumes were calculated using previously established viability thresholds and final infarct volumes ascertained with 2,3,5-triphenyltetrazolium chloride (TTC) staining. Serial MRI demonstrated spontaneous reperfusion of initially hypoperfused MCA regions accompanied by substantial reduction of initial ADC and CBF lesions and gradual recovery of neurological outcome. Recovery rates of CBF/ADC abnormalities differed among ROIs. Functional magnetic resonance imaging showed persistent tissue dysfunction after the recovery of the CBF/ADC lesions. This study may facilitate our understanding of the pathophysiological mechanisms by which early, spontaneous reperfusion affects tissue fate and neurological function.     

Differential recovery of multimodal MRI and behavior after transient focal cerebral ischemia in rats.

The association between recovery of brain function and behavior after transient cerebral ischemia in animals and humans is incompletely characterized. Quantitative diffusion- (DWI), perfusion- (PWI), T(2)-weighted (T(2)WI), and functional magnetic resonance imaging (fMRI) were performed before, during, and up to 1 day after 20-mins transient middle cerebral artery occlusion (tMCAO; n=6) or sham operation (n=6) in male Sprague-Dawley rats. Viability thresholds were employed to calculate diffusion, perfusion, and T(2) lesion volumes. Region of interest analysis was used to evaluate structural and functional MR signal changes within the sensorimotor network, which were then related to corresponding behavioral measures. Post-mortem 2,3,5-triphenyltetrazolium chloride (TTC) staining was performed 24 h after ischemia. Transient middle cerebral artery occlusion produced lesions on DWI and PWI, which fully recovered by 30 mins after reperfusion. Ipsilesional fMRI responses to hypercapnia and forepaw stimulation were significantly impaired after ischemia and did not fully normalize until 3 and 24 h after tMCAO, respectively. No abnormalities were observed on imaging or TTC at 24 h despite significant behavioral dysfunctions including contralesional forelimb impairment and ipsilesional neglect. No MRI, behavioral, or TTC anomalies were observed in sham-operated rats. There were no significant correlations between MRI parameters, behavior, and TTC in either group. Together, these results suggest that normal findings on diffusion, perfusion, and T(2) imaging shortly after transient ischemia may not indicate normal tissue status as indicated by fMRI and behavior, which may help explain the persistence of neurologic deficits in patients with normal conventional MRI after cerebral ischemia.     

Cerebral tissue repair and atrophy after embolic stroke in rat: A magnetic resonance imaging study of erythropoietin therapy

Using magnetic resonance imaging (MRI) protocols of T₂‐, T₂*‐, diffusion‐ and susceptibility‐weighted imaging (T2WI, T2*WI, DWI, and SWI, respectively) with a 7T system, we tested the hypothesis that treatment of embolic stroke with erythropoietin (EPO) initiated at 24 hr and administered daily for 7 days after stroke onset has benefit in repairing ischemic cerebral tissue. Adult Wistar rats were subjected to embolic stroke by means of middle cerebral artery occlusion (MCAO) and were randomly assigned to a treatment (n = 11) or a control (n = 11) group. The treated group was given EPO intraperitoneally at a dose of 5,000 IU/kg daily for 7 days starting 24 hr after MCAO. Controls were given an equal volume of saline. MRI was performed at 24 hr and then weekly for 6 weeks. MRI and histological measurements were compared between groups. Serial T2WI demonstrated that expansion of the ipsilateral ventricle was significantly reduced in the EPO‐treated rats. The volume ratio of ipsilateral parenchymal tissue relative to the contralateral hemisphere was significantly increased after EPO treatment compared with control animals, indicating that EPO significantly reduces atrophy of the ipsilateral hemisphere, although no significant differences in ischemic lesion volume were observed between the two groups. Angiogenesis and white matter remodeling were significantly increased and occurred earlier in EPO‐treated animals than in the controls, as evident from T2*WI and diffusion anisotropy maps, respectively. These data indicate that EPO treatment initiated 24 hr poststroke promotes angiogenesis and axonal remodeling in the ischemic boundary, which may potentially reduce atrophy of the ipsilateral hemisphere. © 2010 Wiley‐Liss, Inc.     

Neuroprotection by oxygen in acute transient focal cerebral ischemia is dose dependent and shows superiority of hyperbaric oxygenation

The neuroprotective effect of oxygen after acute stroke in rats has been shown previously. However, the question of optimal dosing still remains unanswered. Thus, we investigated the use of oxygen at different concentrations by either normobaric oxygenation (NBO) or hyperbaric oxygenation (HBO) at different pressures in a model of transient ischemia/reperfusion in rats. Animals underwent 90 min of middle cerebral artery occlusion (MCAO) followed by 90 min of reperfusion before oxygen treatment. Oxygen was applied either by NBO (100% O(2); 1.0 absolute atmosphere, ATA) or HBO (100% O(2); 1.5, 2.0, 2.5 or 3.0 ATA) for 1 h. Primary endpoints were infarct volume and clinical outcome measured 24 h and 7 days following the MCAO. A statistically significant and long-lasting reduction in infarct volume was seen in the HBO 2.5 ATA and 3.0 ATA groups over a period of 7 days. The reduced infarct volume was accompanied with a statistically significant improvement in clinical outcome in the high-dose oxygen-treated groups. The presented data indicate that oxygen is a highly neuroprotective molecule in transient focal cerebral ischemia in rats, when applied early and at high doses. The effect is dose dependent and shows a superiority of HBO over NBO, when the primary endpoints infarct volume reduction and clinical outcome are analyzed. These data are important for the development of new acute stroke treatment studies in humans.     

Feasibility of establishing cerebral ischemia models by using aerocyst-blocking bilateral ascending pharyngeal artery of piglets Imaging assessment

BACKGROUND: The cerebral ischemia and ischemia/reperfusion animal models are used to simulate the human cerebrovascular diseases is one of the popular topics of neurological science recently. To study the pathophysiology, pathogenesis, prophylaxis and treatment of ischemic cerebrovascular diseases and to establish the ideal animal model that is the most similar to the human cerebral ischemia, are the topics that the people generally cared about. OBJECTIVE: To evaluate the effects of aerocyst-blocking bilateral ascending pharyngeal artery on the establishment of cerebral ischemia models by using digital subtraction angiography (DSA), magnetic resonance diffusion-weighted imaging (DWI) and magnetic resonance perfusion-weighted imaging (PWI). DESIGN: Repetitive measure animal experiment. SETTING: Zhongshan Hospital Affiliated to Dalian University. MATERIALS: The experiment was carried out in the Animal Laboratory (Provincial Laboratory), Zhongshan Hospital of Dalian Univeristy from January to May 2006. A total of 14 domestic piglets, of 6 months old, weighing 12–15 kg, of either gender, were selected from Animal Experimental Center, Dalian University. Multistar T.O.P digital subtraction angiography machine was provided by Siemens Company, German. METHODS: Aerocyst-blocking bilateral ascending pharyngeal artery was used to establish cerebral ischemia models. And then, Multistar T.O.P. DSA was used for imaging of cerebral vessels before blocking, during blocking and at 0.5 and 2 hours after ischemia perfusion. GE Signa 1.5 T supraconduction magnetic resonance imaging was used for DWI examination; in addition, PWI was used based on focal sites and areas. Otherwise, magnetic resonance imaging (MRI) was used to detect signal changes of T1WI and T2WI in ischemic areas. MAIN OUTCOME MEASURES: Analytic results of DSA, DWI, PWI and MRI. RESULTS: All 14 experimental piglets were involved in the final analysis. ① DSA: The blood flow of bilateral ascending pharyngeal arteries and its branch were blocked at blocking phase, which restored 0.5 and 2 hours after reperfusion. ② DWI and PWI: There were no observable abnormalities in PWI and DWI at pre-blocking. Abnormal increased signals were found on both DWI and PWI at during and post-blocking. There were reduction in ADC and rCBF and delay in rTTP at all time points except pre-blocking. ③ MRI: There were no abnormal signals observable at any time of pre- and post-blocking in T1WI and T2WI. CONCLUSION: It is feasible to establish this kind of animal experimental models, and it can simulate the ischemic state; meanwhile, the existence and extent can be showed directly by DSA, DWI, and PWI.     

Dynamic susceptibility contrast-enhanced perfusion MR imaging at 1.5 T predicts final infarct size in a rat stroke model

The purpose of the present animal experiment was to determine whether source images from dynamic susceptibility contrast-enhanced perfusion weighted imaging (DSC-PWI) at a 1.5T MR scanner, performed early after photochemically induced thrombosis (PIT) of cerebral middle artery (MCA), is feasible to predict final cerebral infarct size in a rat stroke model. Fifteen rats were subjected to PIT of proximal MCA. T2 weighted imaging (T2WI), diffusion-weighted imaging (DWI), and contrast-enhanced PWI were obtained at 1 h and 24 h after MCA occlusion. The relative lesion size (RLS) was defined as lesion volume/brain volume x 100% and measured for MR images, and compared with the final RLS on the gold standard triphenyl tetrazolium chloride (TTC) staining at 24 h. One hour after MCA occlusion, the RLS with DSC-PWI was 24.9 +/- 6.3%, which was significantly larger than 17.6 +/- 4.8% with DWI (P < 0.01). At 24 h, the final RLS on TTC was 24.3 +/- 4.8%, which was comparable to 25.1 +/- 3.5%, 24.6 +/- 3.6% and 27.9 +/- 6.8% with T2WI, DWI and DSC-PWI respectively (P > 0.05). The fact that at 1 h after MCA occlusion only the displayed perfusion deficit was similar to the final infarct size on TTC (P > 0.05) suggests that early source images from DSC-PWI at 1.5T MR scanner is feasible to noninvasively predict the final infarct size in rat models of stroke.     

依托咪酯预处理对大鼠局灶性脑缺血-再灌注损伤的保护作用

目的 探讨依托咪酯预处理对脑缺血-再灌注损伤的保护作用。方法 18只雄性SD大鼠,随机均分为3组,即脑缺血-再灌注组、依托咪酯预处理组、脂微球对照组。采用颈内动脉线栓栓塞致大脑中动脉阻塞模型,监测肛温及血糖,并于再灌注24h后断头处死动物,取大脑切片行2,3,5-氯化三苯基四氮唑染色,测量并计算脑梗死容积百分比。结果 依托咪酯预处理组脑梗死百分比明显低于脂微球对照组（P＜0.01）,低于缺血-再灌注组（P＜0.05）。但缺血-再灌注组与脂微球对照组相比差异无统计学意义。结论 依托咪酯预处理后可明显减小大鼠局灶性脑缺血-再灌注损伤后的脑梗死面积。     

大鼠局灶性脑缺血损伤后半暗带区锌离子的变化

目的观察大鼠局灶性脑缺血再灌注后半暗带区锌离子的变化,探讨锌离子在脑缺血再灌注损伤中的可能作用。方法将28只SD大鼠随机分为假手术组(n=12)和大脑中动脉梗死(MCAO)组(n=16),以线栓法制作大鼠MCAO模型。分别于再灌注0h、3h、12h和24h时处死大鼠,取脑组织行TTC染色检测梗死体积,并制作脑组织冷冻切片,采用Newport Green(NG)染色法计数半暗带区NG阳性细胞数目并检测其平均荧光强度,分析NG阳性细胞数目与脑梗死体积的相关性。结果 (1)假手术组大鼠脑组织无梗死灶,也未见NG染色阳性细胞。MCAO组大鼠随再灌注时间延长脑梗死体积增大(均P<0.01),脑缺血半暗带区域NG阳性染色细胞数目随再灌注时间延长递增(均P<0.01)。各时间点间NG染色阳性细胞平均荧光强度无统计学差异(P>0.05)。(2)MCAO组大鼠脑切片NG阳性细胞数目与脑梗死体积比率呈正相关(r=0.88,P<0.01)。结论锌离子可能参与了脑缺血再灌注损伤的过程。     

小型猪脑缺血模型的建立及影像学评价

目的:建立小型猪脑缺血模型,并通过数字减影血管造影(DSA)、磁共振弥散加权成像(DWI)、磁共振灌注加权成像(PWI)进行评价。方法:6月龄小型猪14头采用双侧咽升动脉气囊阻断法制作脑缺血模型,于阻断前、阻断期及再灌注0.5h、2h分别给予DSA、DWI、PWI和MRI评价。结果:阻断期DSA可见双侧咽升动脉及其分支血管血流阻断,再灌后0.5h及2h双侧咽升动脉及其分支血管血供恢复;阻断前DWI、PWI均未见异常,阻断期及再灌注各时间点DWI、PWI发现异常高信号,表观弥散系数(ADC)值和局部脑血流(rCBF)下降,达峰时间(rTTP)延迟;T1WI和T2WI在阻断前、阻断期和再灌后各时间点均未发现异常信号。结论:通过磁共振影像学评价证明双侧咽升动脉气囊阻断法制作小型猪脑缺血模型是稳定的、可重复的,此方法可造成程度较为一致的小型猪缺血性脑损伤。     

磁共振弥散加权成像评价机械性取栓的实验研究

目的 应用磁共振弥散加权成像(DWI)技术评价机械性取栓治疗栓塞性脑梗死的疗效。 方法 40只新西兰兔颈内动脉注入血凝块栓子制备急性栓塞性脑梗死模型后按随机数字表法分为非治疗组（不做任何治疗）、6h机械取栓组、8h机械取栓组、12h机械取栓组（分别于制模成功后6h、8h、12h在DSA导引下经股动脉插管机械取栓）,每组10只,各组分别在6h、8h、12h、24h行DWI并计算各时段表观弥散系数(ADC)和梗死体积。 结果 兔脑梗死超急性期（6 h内）均在DWI上显示缺血区,表现为高信号,在T1WI、T2WI上表现为正常信号;T1WI、T2WI及DWI对急性期(24h内)脑梗死的检出率差异有统计学意义(P＜0.05)。非治疗组、12h机械取栓组在急性期内ADC值逐渐降低,梗死体积逐渐扩大,而6h、8h机械取栓组在急性期取栓后ADC值逐渐上升,梗死体积缩小。梗死后24h,与非治疗组和12h机械取栓组比较,6h和8h机械取栓组ADC值较高,梗死体积较低,差异均有统计学意义(P＜0.05)。 结论 栓塞性脑梗死早期机械性取栓效果显著,DWI是动态观察急性脑梗死治疗效果的敏感影像学手段。     

Neuroprotective effects of hyperbaric oxygen treatment in experimental focal cerebral ischemia are associated with reduced brain leukocyte myeloperoxidase activity

OBJECTIVE: Hyperbaric oxygen (HBO) reduces cerebral infarct size after middle cerebral artery occlusion (MCAO) in rats through an unknown mechanism. In other forms of injury, cellular protection with HBO is associated with diminished infiltration of polymorphonuclear neutrophils (PMN). We hypothesized that HBO given prior to or after MCAO reduces PMN infiltration into the brain, and that decreased PMN infiltration is associated with improved functional and anatomic outcome. METHODS: Forty rats underwent MCAO and were randomized to pretreatment with HBO (3 ATA) immediately prior to (n=13), or posttreatment immediately after surgery (n=12), or to control (air 1 ATA) (n=15). Five rats underwent sham surgery. Neurologic outcome was measured at 24 h in all animals. Brain myeloperoxidase (MPO) activity (n=22) and infarct volume (n=23) were determined. RESULTS: MPO activity was significantly higher in controls (mean 0.28, 95% C.I. 0.17-0.38) than in the HBO pretreatment group (0.12, 0.08-0.16), HBO posttreatment group (0.16, 0.13-0.19), and the sham group (0.02, -0.02 to 0.05). HBO treated animals also had better neurologic outcomes (pretreatment 1.5, 0.9-2.1, posttreatment 2.6, 2.0-3.2) and smaller infarcts (pretreatment 27%, 18-37%, posttreatment 28%, 19-37%) than controls (neurologic outcome 3.7, 3.1-4.4, infarct volume 39%, 30-48%). Neurologic outcomes correlate better with MPO activity (R(2)=0.75) than with infarct volume (R(2)=0.25). CONCLUSION: These data confirm the neuroprotective effects of HBO in cerebral ischemia and suggest that the mechanism of this action may involve inhibition of PMN infiltration in the injured brain.     

高压氧预处理可对大鼠局灶性脑缺血再灌注损伤的保护作用

目的研究短期高压氧预处理后是否可减轻大鼠局灶性脑缺血再灌注损伤。方法选取成年雄性Wister大鼠,采用连续5d,每天1次,3.0ATA,100%O2高压氧(HBO)预处理,每次60min,末次预处理后24h,运用改良的经典线栓法制作MCAO模型,再灌注2h。将实验大鼠分为假手术组、MCAO组、HBO+MCAO组(n=5)。造模后24h观察各组动物的一般精神状态及体重变化情况、用Rogers DC and Hunter AJ描述的神经功能7分评分法对神经功能损伤进行评估,TTC染色测梗死面积,并对脑组织进行石蜡切片,行Nissl、TUNEL染色,利用显微镜对神经细胞进行计数。结果假手术组无神经功能缺失,TTC染色未见梗死灶,镜下观察未见坏死细胞。MCAO组和HBO+MCAO组均有不同程度的神经功能缺损,且HBO+MCAO组神经功能缺失较MCAO组轻;TTC染色MCAO组的梗死面积明显大于HBO+MCAO组;镜下观察,MCAO组梗死区内尼氏小体明显少于HBO+MCAO组。结论短期高压氧预处理后可减轻大鼠局灶性脑缺血再灌注损伤。     

高压氧治疗时机对家兔实验性局部脑缺血治疗效果的影响及微透析监测研究

目的 观察高压氧(HBO)治疗时机对家兔实验性局部脑缺血治疗效果的影响.方法 75只家兔按随机数字表法平均分为3组,每组25只,即大脑巾动脉闭塞(MCAO)组:右侧大脑中动脉阻断.不行HBO治疗;MCAo+HBO组:右侧大脑巾动脉阻断后即予HBO治疗;MCAO+DHBO组:右侧大脑巾动脉阻断7d后行HBO治疗.动物放入HBO舱(100%O2,250 kPa,1 h/d)行HBO治疗30 d.MCAO后第1天、第3天、第10天、第30天观察各组动物的行为学变化、脑梗死体积,并采用微透析技术分析家兔缺血脑组织细胞间液中的葡萄糖、乳酸、丙酮酸、乳酸/丙酮酸比值以及谷氨酸水平的变化.结果 缺血后MCAO+HBO组行为学评分较其他组低;第3天至第30天,MCAO+HBO组脑梗死体积低于其他两组,差异有统计学意义(P<0.05).微透析分析能量代谢指标中乳酸丙酮酸比值变化最为明显.其中缺血后1 d和3 d右侧脑组织间液中MCAO+HBO组较其他两组降低,差异有统计学意义(P<0.05).缺血后家兔脑组织间液中谷氨酸浓度升高,3d时逐渐下降,缺血后1 d和3d右侧腩组织间液中MCAO+HBO组较其他两组降低,差异有统计学意义(P<0.05).结论 HBO治疗能通过改善神经组织的能量代谢,减轻兴奋性氨基酸毒性作用,改善缺血缺氧对神经的损害;而HBO治疗脑梗死应尽早进行.     

高压氧预处理减少局灶性脑缺血后泛素化蛋白聚集

目的探讨泛素-蛋白酶体系统在重复高压氧（HBO）预处理导致的脑缺血耐受中所起的作用。方法采用大脑中动脉阻闭（MCAO）制备大鼠局灶性脑缺血模型,将33只SD大鼠随机分为假手术组（Sham）组、MCAO组和HBO组,分别观察各组大鼠脑梗死灶的大小和神经功能学评分,并用免疫组织化学染色检测再灌注2h、24h时相点大鼠脑组织CA1区异常泛素化蛋白聚集的变化。结果 HBO组脑梗死容积小于MCAO组,差异有统计学意义（P〈0.05）,其神经功能学评分也明显优于MCAO组（P〈0.05）。再灌注各时相点,HBO组泛素化蛋白聚集明显少于MCAO组（P〈0.05）。结论高压氧预处理所诱导的脑缺血耐受的机制可能与泛素化蛋白聚集降低有关。     

Volumetric evaluation of the ischemic lesion size with serial MRI in a transient MCAO model of the rat: comparison of DWI and T1WI

Magnetic resonance imaging (MRI) is applied in many studies on experimental cerebral ischemia in rodents to monitor the temporal evolution of ischemic damage. We report a protocol to evaluate the infarct size after middle cerebral artery occlusion with reperfusion (MCAO/R) in male Wistar rats. Imaging was performed with a 2.35 T scanner and we focused on diffusion-weighted imaging (DWI), T2-weighted imaging (T2WI) and postcontrast T1-weighted imaging (T1WI). We show the detailed procedure of volumetry, the contrast-to-noise ratio (CNR) and the intraindividual variability of infarct and hemispheric volumes at different reperfusion times. The presented method is of low variability if image contrast between ischemic and nonischemic tissue is very high, which is the case not only for all sequences at 8 and 12 h of reperfusion but also for DWI after 3 and 5 h of reperfusion. Furthermore, we describe the so-called mismatch region of lesion sizes depicted on DWI and postcontrast T1WI that suffers from cytotoxic edema but lacks contrast enhancement.     

Further characterisation of a thromboembolic model of stroke in the rat

We have used magnetic resonance imaging (MRI) techniques to characterise a rat model of thromboembolic stroke. The consequences of acute perfusion deficit associated with a middle cerebral artery occlusion (MCAo) by a newly formed thrombus was mapped by interrogation of the tissue oxygenation status using gradient echo methods and production of T2* maps. Final infarct size was subsequently assessed at 24-h post-ischaemia by histology with 2,3,5-triphenyltetrazolium chloride (TTC) staining. Animals displayed an infarct volume of 178.7+/-84.2 mm(3) (mean+/-S.D.) with a large coefficient of variation (47%) and range of values (85.6--265.5 mm(3)). This variability provided us with an opportunity to assess the relationships between early imaging observations and eventual infarct size. For a single cerebral slice, at the centre of the MCA territory, a relationship between the area of reduced T2* at 1 and 2 h post MCAo correlated highly with final lesion area (Spearman rank correlation, r=0.98, P<0.01, n=9). Lesion volumes in the thromboembolic MCAo model were compared with a 120-min occlusion, 22-h reperfusion protocol using an intraluminal thread MCAo approach. For the thromboembolic model, the total lesion volume was found to be smaller (178.7+/-84.2 vs. 243.3+/-50.1 mm(3), mean+/-S.D., Student's t-test P=0.046) and showed a greater variability (coefficient of variations: 47% vs. 21%). These data underline the relative variability of this embolic model and provide important preliminary information regarding the value of early changes in T2* in predicting eventual infarct size.     

单次9小时高压氧超早期治疗对大鼠脑梗死体积的影响

目的 本研究主要观察高压氧（HBO）单次9 h超早期治疗对永久性大脑中动脉阻塞（MCAO）大鼠脑梗死体积的影响。方法 制作SD大鼠永久性MCAO模型,随机分为对照组、HBO组,HBO组大鼠于模型制备成功后3 h予单次9 h HBO治疗,压力0.2 MPa。模型成功后13 h、5 d,分别将大鼠脑组织进行2,3,5苯四氮唑（TTC）染色测定梗死体积,免疫组织化学染色测定脑组织中血管内皮生长因子（VEGF）的表达情况。结果 （1）13 h时,两组大鼠脑梗死体积相差不大（P >0.05）;5 d时,对照组大鼠脑梗死体积较13 h时增大（P <0.05）,而HBO组变化不大（P >0.05）,组间比较,HBO组较对照组脑梗死体积缩小（P <0.05）。（2）13 h时,对照组和HBO组VEGF均有表达,两组间差异无统计学意义（P >0.05）;5 d时,对照组VEGF表达较13 h时明显减少（P <0.01）,而HBO组VEGF表达明显高于13 h,而且显著高于对照组5 d水平（P <0.01）。结论 单次9 h HBO超早期治疗可缩小大鼠脑梗死体积,其机制可能与HBO提高内源性VEGF表达有关。