T2-weighted magnetic resonance imaging of cerebrovascular reactivity in rat reversible focal cerebral ischemia

Cerebrovascular carbon dioxide (CO₂) reactivity is an important hemodynamic index in cerebrovascular disease. In the present study T2^*-weighted magnetic resonance image (T2^*WI) was evaluated as a non-invasive method to investigate changes in CO₂ reactivity. Fourteen rats were subjected to permanent or, 30 and 90 min of temporary middle cerebral artery occlusion. A series of T2^*WIs and diffusion-weighted magnetic resonance images (DWI) was performed hourly under normo- and hypercapnic conditions. Triphenyltetrazolium chloride (TTC) staining of brain sections was obtained at the end of experiment to evaluate ischemic damage. During ischemia, a 4–6% signal increase upon hypercapnia was observed on T2^*WI in the non-ischemic hemisphere, while no such reactivity was seen in the putamen and cortex ipsilateral to the MCA occlusion. After reperfusion, CO₂ reactivity recovered in the putamen and cortex in the 30 min ischemia group and in the cortex alone of the 90 min ischemia groups. The areas with irreversible CO₂ reactivity dysfunction coincidentally revealed no recovery on DWI and lack of TTC staining. The results indicate that T2^*WI can be used to monitor changes in CO₂ reactivity after various ischemic insults that may indicate tissue viability.     

Transient and permanent resolution of ischemic lesions on diffusion-weighted imaging after brief periods of focal ischemia in rats : correlation with histopathology

BACKGROUND AND PURPOSE: The early ischemic lesions demonstrated by diffusion-weighted imaging (DWI) are potentially reversible. The purposes of this study were to determine whether resolution of initial DWI lesions is transient or permanent after different brief periods of focal brain ischemia and to evaluate histological outcomes. METHODS: Sixteen rats were subjected to 10 minutes (n=7) or 30 minutes (n=7) of temporary middle cerebral artery occlusion or sham operation (n=2). DWI, perfusion-weighted imaging (PWI), and T(2)-weighted imaging (T(2)WI) were performed during occlusion; immediately after reperfusion; and at 0.5, 1.0, 1.5, 12, 24, 48, and 72 hours after reperfusion. After the last MRI study, the brains were fixed, sectioned, stained with hematoxylin and eosin, and evaluated for neuronal necrosis. RESULTS: No MRI or histological abnormalities were observed in the sham-operated rats. In both the 10-minute and 30-minute groups, the perfusion deficits and DWI hyperintensities that occurred during occlusion disappeared shortly after reperfusion. The DWI, PWI, and T(2)WI results remained normal thereafter in the 10-minute group, whereas secondary DWI hyperintensity and T(2)WI abnormalities developed at the 12-hour observation point in the 30-minute group. Histological examinations demonstrated neuronal necrosis in both groups, but the number of necrotic neurons was significantly higher in the 30-minute group (95+/-4%) than in the 10-minute group (17+/-10%, P<0.0001). CONCLUSIONS: Transient or permanent resolution of initial DWI lesions depends on the duration of ischemia. Transient resolution of DWI lesions is associated with widespread neuronal necrosis; moreover, permanent resolution of DWI lesions does not necessarily indicate complete salvage of brain tissue from ischemic injury.     

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.     

Effect of the reperfusion after cerebral ischemia in neonatal rats using MRI monitoring

Cerebral hypoxia-ischemia is an important cause of brain injury in the newborn infant. Our purpose was to study magnetic resonance (MR) imaging changes in P7 rat brains submitted to permanent or reversible ischemia. Ischemia was induced by permanent electro-cauterization of the middle cerebral artery combined with a permanent or a transient (50 min) common carotid artery occlusion. The early events during ischemia and reperfusion were investigated by T2-weighted images (T2WI) at 1 and 3 h and by serial diffusion-weighted images (DWI) during 3 h in a 7 T magnet with a standard weighted diffusion sequence (b=1282.04 s mm(-2)) and a SEMS sequence. Within the first hour after MCA occlusion, the T2WI areas of contrast enhancement increased to a mean volume of 12.9+/-6.4%, a steady state still detected at 3 h after the ischemic onset (10.5+/-2.5%). Contrast enhancement in DWI increased as soon as 15 min of ischemia in all animals up to 50 min after CCA occlusion. In permanent ischemia, DWI abnormalities volume then increased more slowly from 50 min to 3 h after CCA occlusion (+25%, n=5). In reversible ischemia, the DWI abnormalities volume either moderately decreased and reached a plateau (-8.4%, n=4) or dramatically decreased (-53.0%, n=3). Both T2WI and DWI evidenced a "patchy" pattern of recovery as also shown on cresyl violet-stained sections. In contrast to the adult, early ischemic injury in P7 rat brains is detected as an increase in hyper-intensities both in T2WI and DWI. Our data indicate that reperfusion is able to block edema evolution after neonatal stroke and that early T2WI and more accurately DWI allow to distinguish between different patterns of injury in reversible ischemia.     

大鼠大脑中动脉缺血/再灌注模型中Caspase-3的表达

目的 研究Caspase-3在缺血性脑损伤中的作用，进一步探讨缺血性脑血管病的分子机制。方法 用Belayev改良的Longa线栓法制备大鼠局灶性大脑中动脉(MCA)缺血／再灌注模型，TTC染色观察梗死灶的形成，分别用原位杂交及免疫组化技术检测鼠脑中Caspase-3 mRNA与活性蛋白的表达。结果 缺血2小时再灌注24小时，TTC染色见明显的梗死灶形成，正常脑组织、假手术组及MCAO缺血对侧脑中有少量的Caspase-3 mRNA表达，但活性蛋白几无表达；再灌注24小时后，缺血侧脑中Caspase-3 mRNA表达明显增强，蛋白质活化增多，再灌注48小时进一步增加。结论 细胞凋亡机制参与了缺血后迟发性神经元死亡，Caspase-3在其中起重要作用。     

Reversible focal ischemic injury demonstrated by diffusion-weighted magnetic resonance imaging in rats.

BACKGROUND AND PURPOSE: Diffusion-weighted magnetic resonance imaging (DWI) can quantitatively display focal brain abnormalities within minutes after the onset of ischemia. We performed the present study to determine the effects of 1 and 2 hours of temporary ischemia on DWI. METHODS: We examined DWI and T2-weighted magnetic resonance images (T2WI) during and after 1 and 2 hours of temporary middle cerebral artery occlusion in rats (n = 10 for each group). In a subgroup of four animals from each group, we employed perfusion magnetic resonance imaging to monitor cerebral perfusion. Neurological outcome and infarct size after survival for 24 hours were compared between the groups and correlated with DWI and T2WI studies. RESULTS: Perfusion studies qualitatively documented hypoperfusion and reperfusion during and after temporary occlusion. Lesion size on DWI during reperfusion was significantly less than that during ischemia for 1 (55% decline, p less than 0.02) but not 2 hours of occlusion. The DWI signal intensity ratio (intensity compared with that in the contralateral homologous area) just before withdrawal of the occluder was significantly less in regions where the hyperintensity disappeared after withdrawal than in regions with persistent hyperintensity (p less than 0.002). The T2WI studies revealed few or no abnormalities, except after 2 hours of occlusion. The neurological outcome was significantly better in the 1-hour than in the 2-hour group (p less than 0.05). Postmortem infarct volume was significantly smaller in the 1-hour group than in the 2-hour group (p less than 0.05). The postwithdrawal DWI accurately predicted infarct size (R = 0.96, p less than 0.0001). CONCLUSIONS: The present study indicates that DWI can rapidly display not only irreversible but also reversible ischemic brain damage and enhances the importance of DWI as a diagnostic modality for stroke.     

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.     

Temporal evolution of ischemic injury evaluated with diffusion-, perfusion-, and T2-weighted MRI

OBJECTIVE: Ischemic lesions seen on diffusion-weighted imaging (DWI) are reversible if reperfusion is performed within minutes after the onset of ischemia. This study was designed to determine whether acute reversibility of DWI abnormalities is transient following brief temporary focal brain ischemia and to characterize the temporal evolution of in vivo ischemic lesions. METHODS: Eight rats were subjected to 30 minutes of temporary middle cerebral artery occlusion and underwent diffusion-, perfusion-, and T2-weighted MRI during occlusion; immediately after reperfusion; 30, 60, and 90 minutes after reperfusion; and 12, 24, 48, and 72 hours after reperfusion. Average apparent diffusion coefficient (ADCav) values and the cerebral blood flow index (CBFi) ratio were calculated in both the lateral caudoputamen and overlying cortex at each time point. The size of the in vivo ischemic abnormalities was calculated from the ADCav and the T2 maps. Postmortem triphenyltetrazolium chloride (TTC) staining was used to verify ischemic injury. RESULTS: Both the CBFi ratio and ADCav values declined significantly in the two regions during occlusion. The CBFi ratio recovered immediately after reperfusion and remained unchanged over 72 hours. However, ADCav values returned to normal at 60 to 90 minutes and secondarily decreased at 12 hours after reperfusion as compared with those in the contralateral hemisphere. The extent of the in vivo ischemic lesions maximized at 48 hours and was highly correlated with TTC-derived lesion size. CONCLUSIONS: Acute recovery of initial ADCav-defined lesions after reperfusion is transient, and secondary ADCav-defined lesions develop in a slow and delayed fashion.     

Aquaporin-4 gene silencing protects injured neurons after early cerebral infarction

Aquaporin-4 regulates water molecule channels and is important in tissue regulation and water transportation in the brain. Upregulation of aquaporin-4 expression is closely related to cellular edema after early cerebral infarction. Cellular edema and aquaporin-4 expression can be determined by measuring cerebral infarct area and apparent diffusion coefficient using diffusion-weighted imaging(DWI). We examined the effects of silencing aquaporin-4 on cerebral infarction. Rat models of cerebral infarction were established by occlusion of the right middle cerebral artery and si RNA-aquaporin-4 was immediately injected via the right basal ganglia. In control animals, the area of high signal intensity and relative apparent diffusion coefficient value on T2-weighted imaging(T2WI) and DWI gradually increased within 0.5–6 hours after cerebral infarction. After aquaporin-4 gene silencing, the area of high signal intensity on T2 WI and DWI reduced, relative apparent diffusion coefficient value was increased, and cellular edema was obviously alleviated. At 6 hours after cerebral infarction, the apparent diffusion coefficient value was similar between treatment and model groups, but angioedema was still obvious in the treatment group. These results indicate that aquaporin-4 gene silencing can effectively relieve cellular edema after early cerebral infarction; and when conducted accurately and on time, the diffusion coefficient value and the area of high signal intensity on T2 WI and DWI can reflect therapeutic effects of aquaporin-4 gene silencing on cellular edema.     

磁共振不同成像序列对大脑中动脉主干闭塞的诊断价值

目的研究磁共振（MRI）不同成像序列在诊断大脑中动脉（MCA）主干闭塞中的价值。方法选择发病48h内行头颅MRI检查，并选择磁共振血管成像（MRA）显示单侧MCA主干闭塞的患者作为研究对象，观察T1加权像、T2加权像、FLAIR成像的MCA主干闭塞征象。结果共有41例脑梗死或TIA患者入组，T2WI成像显示侧裂池血管流空影减少和FLAIR成像侧裂池显示等或高信号血管影对MCA主干闭塞的诊断灵敏度较其他3个征象高，分别为78．0％和75．6％，诊断特异度均为100％，两者的诊断正确率较其他3个征象高。结论所有患者至少观察到1个MCA主干闭塞的MRI征象，其中T2WI成像显示侧裂池血管流空影减少和FLAIR成像显示侧裂池等或高信号血管影对MCA主干闭塞的诊断价值高于其他MRI征象。     

Effect of pretreatment with the calcium antagonist nimodipine on local cerebral blood flow and histopathology after middle cerebral artery occlusion

We used the [¹⁴C]iodoantipyrine autoradiography technique to study the effect of pretreatment with the calcium antagonist nimodipine on local cerebral blood flow (1CBF) in rats that underwent middle cerebral artery (MCA) occlusion. In untreated control animals there were profound localized reductions in 1CBF 30 minutes after MCA occlusion. These were most pronounced in neocortical areas and in the caudate nucleus ipsilateral to the MCA occlusion. In animals pretreated with nimodipine (1 μg · kg^?1 · min^?1 for 30 minutes before and 30 minutes after MCA occlusion), the ipsilateral decrease in 1CBF in cortical regions was significantly less than that in control animals. The drug did not appear to alter 1CBF in the ipsilateral caudate nucleus. Neuropathological quantification of the ischemic damage present 3 hours after occlusion showed thai: nimodipine pretreatment reduced the volume and extent of cellular damage in the periphery but not in the core of the lesion.     

Transient focal ischemia in subhuman primates. Neuronal injury as a function of local cerebral blood flow

Unilateral, transient (30, 60, and 120 minutes (min)) middle-cerebral-artery (MCA) occlusion was induced via transorbital craniotomy in 11 waking subhuman primates. Local cerebral blood flow (LCBF) was calculated from hydrogen clearance curves obtained through the use of intracerebral platinum microelectrodes. Unilateral MCA occlusion decreased LCBF in the territory of the ipsilateral MCA. Within minutes of the arterial occlusion all monkeys developed contralateral neurologic deficits that began disappearing three hours (h) after reopening the MCA. Regional ischemia, followed by 24 h of reperfusion, produced varying degrees of tissue vacuolation which correlated (r = 0.60, p less than 0.01, n = 49) with the percent reduction in LCBF multiplied by the occlusion time. Neurons were classified according to the structural features of their perikaryon. A plot of neuron types versus percent vacuolation suggested that normal neurons become increasingly scalloped under increasingly severe ischemic conditions. The number of scalloped neurons decreased precipitously in areas of marked sponginess coincident with the appearance of irreversibly damaged neurons. Local tissue edema values exceeding 30% correlated with irreversible injury to all neurons in the same area. Regional cerebral ischemia of increasing severity was acompanied by increasing numbers of lethally injured neurons.     

急性脑梗死散在和单一弥散加权成像病损与其供血动脉狭窄的关系

目的 探讨急性脑梗死弥散加权磁共振成像(DWI)上大脑中动脉(MCA)供血区散在性或单一性缺血性病损与其脑供血动脉狭窄或闭塞的关系.方法 回顾性分析73例连续积累的DWI显示一侧MCA供血区脑梗死的病例,入组病例均排除心源性栓塞性脑梗死,所有患者均在发病24 h内进行MRI和MRA等检查,7例患者并进行DSA.采用DWI急性缺血性病损分类方法 分为散在病损组和单一病损组,比较两组的病灶同侧MCA、颈内动脉(ICA)颅内段和颅外段狭窄或闭塞的发生率.结果 散在病损组42例,单一病损组31例.在病损同侧ICA颅外段和MCA闭塞或重度狭窄方面两组差异有统计学意义(28.6%与0,x2=10.6,P=0.001).在病损同侧ICA颅内段并MCA轻中度狭窄方面,两组间差异具有统计学意义(31.0%与9.7%,x2=4.717,P=0.03).散在病损与MCA和(或)ICA严重或多发狭窄呈正相关(OR值为13.7,95%CI:3.6～52.5).在MRA或DSA未发现颅内外大血管狭窄方面,两组间差异具有统计学意义(11.9%与32.3%,x2=4.526,P=0.033).散在病损组与无明显血管狭窄呈负相关(OR值为0.284,95%CI:0.09～0.94).结论 (1)脑梗死急性期DWI显示的MCA区散在性病损患者,MCA和ICA狭窄、甚至闭塞的可能性较大,以ICA颅外段闭塞较为常见;(2)DWI显示单一病损时提示脑供血动脉狭窄程度较轻,范围较局限,小血管病变的可能性相对较高,很少为严重的ICA颅外段狭窄或闭塞.

Abstract：

Objective To investigate the relationship between scattered or single lesion of acute cerebral infarction in middle cerebral artery territory on diffusion-weighted imaging (DWI) and stenosis of middle cerebral artery (MCA) or internal carotid artery (ICA). Methods With exclusion of cardioembolism, 73 consecutive patients with acute cerebral infarction of the unilateral MCA territory on DWI were analyzed. All patients got magnetic resonance imaging (MRI) and angiography (MRA) within 24 hours after onset, and 7 patients also had digital subtraction angiography (DSA). The patients were classified into single lesion group or scattered lesions group according to the DWI findings. The incidence of stenosis or occlusion of ipsolateral MCA, intracranial and extracranial ICA were compared between the two groups. Results 42 patients had scattered lesions and 31 patients had single lesion. The scattered-lesions group had a high incidence of ipsilateral extracranial ICA or MCA occlusion or severe stenosis ( 25.6%versus 0, x2 = 10.6, P = 0.001 ) and a high incidence of ipsilateral intracranial ICA or MCA moderate or mild stenosis (31.0% versus 9.7% ,x2 =4.717, P =0.03 ). A positive correlation was found between the scattered lesions and severe or multifocal stenosis of ipsilateral ICA and MCA ( OR: 13.7, 95% CI: 3.6 to 52.5). There was a low incidence of absence of extra- and intracranial stenosis on MRA or DSA in the scattered-lesions group ( 11.9% versus 32.3%, x2= 4.526, P = 0.033 ). A negative correlation was found between the scattered lesions and absence of large-artery stenosis ( OR: 0.284, 95% CI: 0.09 to 0.94).Conclusions ( 1 ) Patients with acute cerebral infarction and scattered lesions on DWI were more likely to suffer from stenosis or occlusion of ICA or MCA, especially over the extracranial ICA. (2) Patients with single lesion were less likely to have severe or multiple stenosis of MCA and ICA, indicating the relevance of small-vessel pathogenesis.     

Evaluation of 2,3,5-triphenyltetrazolium chloride as a stain for detection and quantification of experimental cerebral infarction in rats

We have evaluated the use of 2,3,5-triphenyltetrazolium chloride (TTC) as an histopathologic stain for identification of infarcted rat brain tissue. The middle cerebral artery (MCA) of 35 normal adult rats was occluded surgically. At various times after surgical occlusion, rats were sacrificed and brain slices were obtained and stained with TTC or hematoxolin and eosin (H & E); the size of the area of infarcted tissue stained by each method was quantified. In rats sacrificed 24 hr after occlusion of the MCA, the size of the area of infarction was 21 +/- 2% of the coronal section for TTC, and 21 +/- 2% for H & E (mean +/- S.D., N = 13). The size of areas of infarction determined by either staining method was not significantly different in area by the paired test, and a significant correlation between sizes determined by each method was found by linear regression analysis (r = 0.91, slope = 0.89, and the y intercept = 4.4%). Staining with TTC is a rapid, convenient, inexpensive, and reliable method for the detection and quantification of cerebral infarction in rats 24 hr after the onset of ischemia.     

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.     

不同时间兔短暂性局灶脑缺血MRI动态演变和病理组织学改变

目的研究兔不同时间短暂局灶脑缺血后MRI(包括DWI、PWI和T2WI)缺血改变的时程,并且评价其组织病理学改变。为短暂性脑缺血发作患者的临床诊断和治疗提供依据。方法60只新西兰白兔分为7、10和30min短暂大脑中动脉阻塞模型和假手术组,各组15只。在阻塞前、阻塞中和再灌注后0.5h、2h、6h、12h、24h、48h、72h对实验动物MRI检查(包括DWI,PWI和T2WI),在MRI检查后于72h时间点进行组织病理学评价。结果在假手术组,无MRI和组织学异常。在7、10和30min组,在阻塞时的灌注不足和DWI高信号于再灌注后消失。此后,在7min组,DWI,PWI和T2WI保持正常,而在15和30min组,于6～12小时观察点出现继发的DWI高信号和T2WI异常。组织学检查显示在三组均有神经元坏死,但是,坏死神经元数目在15和30min组显著高于7min组(P<0.001)。结论于再灌注后DWI信号异常的短暂或持久消失依赖于缺血持续时间。DWI信号异常的短暂消失动物有广泛的神经元坏死;然而,DWI信号异常持久消失并不不表明缺血损伤的脑组织完全恢复。这些结果有助于解释在有些脑缺血后DWI正常的患者神经功能缺失的表现,以及有些经历过TIA的患者表现认知功能改变。     

大脑中动脉区梗死的DWI特点及与其供血动脉狭窄的关系

目的 探讨大脑中动脉(MCA)区脑梗死磁共振扩散加权成像(DWI)成像病灶分布特点及与其供血动脉狭窄程度的关系.方法 回顾性的分析经颅脑磁共振成像(MRI)的DWI序列诊断的急性脑梗死,选择病灶位于MCA分布区,且完善其供血动脉检查,包括头颈部CTA,或颅脑MRA加颈部血管超声的患者108例,排除心源性栓塞、特殊血管病变导致的脑梗死.将梗死按照部位分为腔隙型梗死(SSSI)、皮层下梗死(SI)和混合型梗死(MI),供血动脉分为正常、轻度(50％)、重度(50％)和闭塞.比较不同类型梗死组的供血动脉狭窄的发生率.结果 各种梗死类型的发生率之间差异无统计学意义(x2=1.08,P＞0.05).单纯MCA病变者53例(53/108,49.1％),单纯ICA病变者28例(28/108,25.9％),单纯MCA病变高于单纯ICA病变(x2=12.35,P＜0.01).同侧血管正常者以LI类型的梗死多见,而单纯ICA病变者以MI类型的梗死多见(x2=10.22;10.54,P＜0.01);三种梗死类型在单纯MCA病变患者中差异无统计学意义(x2=0.25,P＞0.05);在单纯MCA病变者中,SI梗死类型多见于MCA闭塞患者(x2=7.45,P＜0.05).LI梗死类型多见于MCA轻度或重度狭窄患者(x2=6.39,P＜0.05).结论 结合DWI和相应血管检查对于明确MCA区动脉粥样硬化性脑梗死的病因和机制有一定帮助.基底节区的腔隙梗死,相应血管检查正常提示小血管病的可能大;MCA存在一定狭窄则可能是穿支受累造成;ICA病变多累及皮层,包括皮层型分水岭区梗死;而不同程度的MCA病变其梗死形态没有本质区别,皮层下梗死更多见MCA闭塞患者.     

Triphenyltetrazolium chloride (TTC) as a marker for ischaemic changes in rat brain following permanent middle cerebral artery occlusion

Triphenyltetrazolium chloride (TTC) was used to delineate ischaemic lesions in the rat brain at various times following middle cerebral artery occlusion. A comparison was made of TTC staining by immersion and perfusion techniques and conventional light microscopy. The lesions were quantified by measuring the ischaemic area at the sections corresponding to 7 mm in front of the AO line (atlas of Konig and Klippel). In animals examined 24 h after middle cerebral artery occlusion (MCAO), the area of infarction was 17.4 +/- 1.3 mm2 on the TTC perfused slices and 17.6 +/- 1.6 mm2 on the TTC immersed slices (mean +/- SEM). By contrast, there was a marked difference between the two TTC methods when tissues were examined at shorter intervals after artery occlusion. In the TTC-perfused animals, there was no significant difference between the mean areas of infarction measured at 5-20 min, 3-4 h, or 24 h post occlusion. Immersion in TTC, however, failed to reveal any consistent ischaemic damage when applied at the earlier post-occlusion times. Conventional histopathology demonstrated minimal lesions at 5-20 min but at 4 h or more the lesions were not significantly different from those demonstrated by TTC perfusion. TTC immersion staining can, thus, only be used as a reliable marker of cerebral ischaemia damage with post-occlusion survival periods of 24 h. TTC perfusion staining gives results not significantly different from histopathology at 4 h or more post-occlusion but at earlier intervals than 24 h it differs significantly from TTC immersion staining.(ABSTRACT TRUNCATED AT 250 WORDS)     

心肌梗死模型家猪存活心肌的磁共振延迟成像评价★

背景：心脏磁共振延迟成像被认为是极有前景的无创性判断心肌存活状态的影像检查手段。目前常用的对比剂Gd-DTPA存在过高或过低评价存活心肌和不可逆性梗死心肌，而坏死亲和性对比剂ECIII-600可以准确地反映坏死心肌的面积。 目的：对比冠脉内注射坏死亲和性对比剂在猪再灌注急性心肌梗死存活心肌诊断中的应用价值。 方法：三四个月龄普通家猪12头，建立急性再灌注心肌梗死动物模型，分别冠脉内注射0.1 mmol/kg Gd-DTPA或 0.005 mmol/kg ECIII-600。胸导R波触发心电门控，T1加权FAST序列，短轴面延迟强化扫描成像。扫描结束后沿短轴面将心脏切成6 mm断面行氯化三苯基四氮唑染色和光镜检查。比较相应层面的MRI延迟强化区和氯化三苯基四氮唑染色所示梗死区的关系。 结果与结论：注射Gd-DTPA的延迟成像10 min时强化区面积与氯化三苯基四氮唑染色相比过高估计梗死心肌面积约21%，30 min时强化区面积与氯化三苯基四氮唑染色结果一致，之后则过低估计坏死心肌的面积；注射ECIII-600的延迟磁共振成像在坏死区显示强烈而持续的对比增强，强化区面积与氯化三苯基四氮唑染色所示心肌梗死面积一致。说明ECIII-600增强磁共振延迟成像可以准确反映急性心肌梗死面积。Gd-DTPA评价心肌梗死面积不稳定，观察时间窗短，心脏磁共振成像应在对比剂注射后1 h以内完成。