人工合成E-选择素治疗鼠局灶脑缺血再灌注损伤的探讨

目的 探讨新的药物有效地治疗急性期脑缺血再灌注损伤。方法 用人工合成Ｅ－ｓｅｌｅｃｔｉｎ Ｌｅｃｔｉｎ Ｄｏｍａｉｎ（以下Ｅ－选择素）Ｎ－末端２３－３０氨基酸残基合成的寡肽（Ｏｌｉｇｏｐｅｐｔｉｄｅ）２ｍｇ／ｋｇ或１０ｍｇ／ｋｇ溶解于生理盐水中,静脉注入自发性高血压大鼠（ＳＨＲ）永久性大脑中动脉／颈总动脉硬化（ＭＣＡ／ＣＣＡ）闭塞或ＭＣＡ／ＣＣＡ闭塞２小时后ＣＣＡ再灌注的模型中。２４小时后,脑梗死体积用计算机扫描计算。结果 在永久性ＭＣＡ／ＣＣＡ闭塞组中脑梗死体积没有差别,在ＭＣＡ／ＣＣＡ闭塞后ＣＣＡ再灌注组中脑梗死体积显著缩小（Ｐ〈０．０１）。结论 Ｅ－选择素能够有效地减少大鼠脑缺血再灌注损伤。     

E—选择素对局灶缺血性脑皮质血流的影响

目的探讨Ｅ－选择素对局灶缺血性脑皮质血流的影响。方法用Ｅ－ｓｅｌｅｃｔｉｎＬｅｃｔｉｎＤｏ－ｍａｉｎ（以下Ｅ－选择素）Ｎ－末端２３－３０氨基酸残基合成的寡肽（Ｏｌｉｇｏｐｅｐｔｉｄｅ）１０ｍｇ／ｋｇ，或伪Ｅ－ｓｅｌｅｃｔｉｎ或等量生理盐水，在ＳＨＲ（自发高血压性大鼠）ＭＣＡ／ＣＣＡ（大脑中动脉／颈总动脉）闭塞２ｈ后ＣＣＡ再灌注的模型中，静脉内缓慢注入，用激光多普勒血流测定仪从ＳＨＲ缺血前１０ｍｉｎ起至ＭＣＡ／ＣＣＡ闭塞２ｈ、ＣＣＡ再灌注后３０ｍｉｎ止，在大脑皮质背侧测定脑血流的变化。结果生理盐水组、伪Ｅ－选择素和Ｅ－选择素组的局部脑血流分别是２３％、２９％和５４％，有统计学意义（Ｐ＜０．０５）。结论Ｅ－选择素能够有效地增加ＳＨＲ缺血再灌注后脑皮质的血流     

NOS抑制剂对缺血再灌注脑组织rCBF及白细胞浸润的 …

目的 应用非选择性ＮＯＳ抑制剂Ｌ－ＮＡＭＥ和选择性ｉＮＯＳ抑制剂ＡＧ治疗鼠大脑中动脉缺血再灌注损伤，通过对脑梗死体积，ｒＣＢＦ和白细胞浸润程度的观察，研究探讨不同类型ＮＯＳ抑制剂治疗脑梗死的机制。方法 采用线栓法制作鼠大脑中动脉缺血再灌注模型，不同缺血及再灌注时间测定脑梗死体积，ｒＣＢＦ，缺血脑组织ＭＰＯ酶活性，结果 应用Ｌ－ＮＡＭＥ（１５ｍｇ／ｋｇ，ｉｐ）不但障碍再灌注后ｒＣＢＦ的恢复，也增加缺     

硫酸镁对大鼠脑缺血再灌流损伤保护作用的研究

目的:探讨ＭｇＳＯ４对大鼠脑缺血再灌流损伤的保护作用。方法:线栓法将ＳＤ大鼠制成脑缺血再灌流模型,分组测定脑组织Ｎａ＋－Ｋ＋－ＡＴＰａｓｅ活性、ＭＤＡ、ＮＯ含量。结果:治疗１组(３００ｍｇ·ｋｇ－１)和治疗２组(６００ｍｇ·ｋｇ－１)与对照组比较,Ｎａ＋－Ｋ＋－ＡＴＰａｓｅ活性增加,ＭＤＡ、ＮＯ含量降低,且治疗２组比治疗１组作用更明显。结论:ＭｇＳＯ４对脑缺血再灌流损伤有保护作用,６００ｍｇ·ｋｇ－１较３００ｍｇ·ｋｇ－１更显著。     

大鼠局灶性脑缺血再灌注模型纹状体内IL—1β和TNF—α动态变 …

目的 观测大鼠局灶性脑缺血再灌注模型缺血侧纹状体区内白细胞介素－１β（ＩＬ－１β）和肿瘤细胞坏死因子－α的动态变化，及甲基强的松龙和榄香烯乳对其的影响。方法 用线栓法阻塞大脑中动脉，用ＥＬＩＳＡ法检测ＩＬ－１β和ＴＮＦ－α。结果 缺血１ｈ再灌注１ｈ后即有ＴＮＦ－α成倍升高，６ｈ达高峰，随后逐渐下降，ＩＬ－１β在再灌注３ｈ升高。缺血后即刻给予３ｍｇ／ｋｇ甲基强的松龙或１０ｍｇ／ｋｇ榄香烯乳可以降低Ｔ     

大鼠局灶性脑缺血再灌注模型纹状体内IL-1β和TNF-α动态变化及药物干预

目的观测大鼠局灶性脑缺血再灌注模型缺血侧纹状体区内白细胞介素－１β（ＩＬ－１β）和肿瘤细胞坏死因子－α（ＴＮＦ－α）的动态变化，及甲基强的松龙和榄香烯乳对其的影响。方法用线栓法阻塞大脑中动脉，用ＥＬＩＳＡ法检测ＩＬ－１β和ＴＮＦ－α。结果缺血１ｈ再灌注１ｈ后即有ＴＮＦ－α成倍升高，６ｈ达高峰，随后逐渐下降；ＩＬ－１β在再灌注３ｈ升高。缺血后即刻给予３ｍｇ／ｋｇ甲基强的松龙或１０ｍｇ／ｋｇ榄香烯乳可以降低ＴＮＦ－α水平，但不影响ＩＬ－１β水平。结论局灶性脑缺血再灌注后有ＩＬ－１β和ＴＮＦ－α的升高，６ｈ达高峰；３ｍｇ／ｋｇ甲基强的松龙或１０ｍｇ／ｋｇ榄香烯乳可以降低缺血区ＴＮＦ－α水平。     

大鼠局灶性脑缺血再灌注后皮层ICAM-1表达增加

目的：研究大鼠局灶性脑缺血再灌注不同时相皮层 ＩＣＡＭ－１变化规律。方法：改良 Ｋｏｉｚｕｍｉ法建立 ＬＭＣＡＯ局灶性脑缺血再灌注模型;ＲＴ－ＰＣＲ和 Ｄｏｔ ｂｌｏｔｔｉｎｇ法分别检测 ＩＣＡＭ－１的转录和翻译水平变化。结果：缺血皮层 ＩＣＡＭ－１ｍＲＮＡ和 Ｉ－ＣＡＭ－１分别于缺血 ２ｈ和再灌注 ２ｈ显著升高,再灌注 １０和 ４６ｈ达高峰,持续 １周仍维持在较高水平。结论：ＩＣＡＭ－１在脑缺血再灌注时表达明显上调,介导白细胞和脑血管内皮细胞的粘附。ＩＣＡＭ－１ 将成为缺血性脑卒中治疗的新突破点。     

大鼠脑缺血再灌注区ICAM-1表达与白细胞浸润的观察及丹参的影响

目的　观察细胞间粘附分子（ Ｉ Ｃ Ａ Ｍ１） 蛋白在大鼠脑缺血再灌注的不同时程脑组织中的表达与中性白细胞浸润程度的关系及丹参对它们的影响。方法　 Ｓ Ｄ大鼠分为３ 组：假手术组、对照组及丹参组。大脑中动脉缺血２ ｈ 再灌注２ ｈ 、１２ ｈ、２４ ｈ 、４８ ｈ 、７２ ｈ 、７ ｄ、１４ ｄ 后,分别进行 Ｉ Ｃ Ａ Ｍ１ 免疫组织化学及组织 Ｈ Ｅ染色。结果　在脑缺血再灌早期,脑微血管内皮细胞 Ｉ Ｃ Ａ Ｍ１ 免疫反应开始逐渐增加,再灌注４８ ｈ 达到高峰,再灌注１４ ｄ 接近正常水平,同时脑缺血区中性白细胞浸润也随之增加,在时程上与 Ｉ Ｃ Ａ Ｍ１ 表达同步。丹参组,再灌注４８ ｈ 后, Ｉ Ｃ Ａ Ｍ１ 免疫阳性血管数及中性白细胞的浸润比同时间对照组明显降低。结论　脑缺血 Ｉ Ｃ Ａ Ｍ１ 的表达与中性白细胞浸润密切相关,丹参能降低 Ｉ Ｃ Ａ Ｍ１ 的表达,抑制中性白细胞的浸润。     

谷氨酸对急性脑缺血再灌注大鼠皮层乙酰胆碱活性影响的在体动态电化学研究

为了研究脑缺血时兴奋性氨基酸与胆碱能神经的关系，采用双侧颈总动脉夹闭（ＣＣＡＯ）的脑缺血动物模型，用乙酰胆碱离子选择性微电极（ＡＣｈ－ＩＳＭｓ）检测皮层ＡＣｈ释放量，观察脑缺血再灌注时谷氨酸对大鼠皮层ＡＣｈ释放量的影响。结果表明：１０－１ｍｏｌ／ＬＧｌｕ对ＡＣｈ－ＩＳＭｓ无干扰作用，在生理状态下不能显著地促进皮层ＡＣｈ的释放，但可使脑缺血３ｍｉｎ时皮层ＡＣｈ释放量较未加Ｇｌｕ组增加５８．１％（Ｐ＜０．０１），再灌注后皮层ＡＣｈ活性恢复减慢。结果提示：Ｇｌｕ协同ＡＣｈ释放的效应在脑缺血时明显放大，推测Ｇｌｕ和ＡＣｈ可能在缺血性脑损伤中有放大的协同作用。     

7—nitro—indazole减小大鼠暂时性局灶性脑梗塞灶范围

目的探讨神经元型一氧化氮合酶（ｎＮＯＳ）在暂时性局灶性脑缺血中的作用。方法用栓线法建立了大脑中动脉阻塞（ＭＣＡＯ）模型的大鼠上，观察特异性ｎＮＯＳ抑制剂７－ｎｉｔｒｏ－ｉｎｄａｚｏｌｅ（７－ＮＩ）对大鼠缺血３ｈ、再灌注３ｈ脑梗塞灶范围的影响。结果７－ＮＩ（２５ｍｇ／ｋｇ）可减小大鼠脑梗塞灶范围，且主要减小大脑皮质梗塞灶，其作用可被Ｌ－精氨酸（３００ｍｇ／ｋｇ）逆转，Ｄ－精氨酸（３００ｍｇ／ｋｇ）则否。结论ｎＮＯＳ产生的ＮＯ在暂时性局灶性脑缺血中起损害作用     

Interrupting reperfusion as a stroke therapy: ischemic postconditioning reduces infarct size after focal ischemia in rats.

Cerebral ischemic preconditioning protects against stroke, but is clinically feasible only when the occurrence of stroke is predictable. Reperfusion plays a critical role in cerebral injury after stroke; we tested the hypothesis that interrupting reperfusion lessens ischemic injury. We found for the first time that such postconditioning with a series of mechanical interruptions of reperfusion significantly reduces ischemic damage. Focal ischemia was generated by permanent distal middle cerebral artery (MCA) occlusion plus transient bilateral common carotid artery (CCA) occlusion. After 30 secs of CCA reperfusion, ischemic postconditioning was performed by occluding CCAs for 10 secs, and then allowing for another two cycles of 30 secs of reperfusion and 10 secs of CCA occlusion. Infarct size was measured 2 days later. Cerebral blood flow (CBF) was measured in animals subjected to permanent MCA occlusion plus 15 mins of bilateral CCA occlusion, which demonstrates that postconditioning disturbed the early hyperemia immediately after reperfusion. Postconditioning dose dependently reduced infarct size in animals subjected to permanent MCA occlusion combined with 15, 30, and 60 mins of bilateral CCA occlusion, by reducing infarct size approximately 80%, 51%, and 17%, respectively. In addition, postconditioning blocked terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end labeling-positive staining, a marker of apoptosis, in the penumbra 2 days after stroke. Furthermore, in situ superoxide detection using hydroethidine suggested that postconditioning attenuated superoxide products during early reperfusion after stroke. In conclusion, postconditioning reduced infarct size, most plausibly by blocking apoptosis and free radical generation. With further study it may eventually be clinically applicable for stroke treatment.     

High-dose methylprednisolone treatment in experimental focal cerebral ischemia

Previous studies using steroids for experimental focal stroke have demonstrated conflicting results, possibly related to dose used or ischemic models employed. In this study we examined high-dose methylprednisolone treatment following permanent and temporary focal cerebral ischemia in the rat. Focal stroke was induced in spontaneously hypertensive rats by permanent right common carotid and either permanent or 3 h of temporary middle cerebral artery (MCA) occlusion. Methylprednisolone (105 mg/kg) was administered intra-arterially. Infarct volume was measured at 24 h after permanent and temporary MCA occlusion. Cerebral edema was determined by measuring right and left hemispheric volumes and water content 24 h after permanent MCA occlusion in one experiment. Methylprednisolone, whether administered in divided doses over 12 h (n = 15 in each group) or a single bolus (n = 9 per group), had no effect on infarct volume after permanent MCA occlusion. Methylprednisolone treatment also had no influence on cerebral edema (n = 9 per group). In two different experiments, methylprednisolone given in divided doses over 12 h (n = 11, n = 25) after temporary MCA occlusion decreased infarct volume (P < 0.05) by 20% compared with saline controls (n = 10, n = 25). High dose methylprednisolone decreased infarct volume following temporary, but not permanent, focal ischemia. The benefit suggests that high dose methylprednisolone may prove useful clinically if reperfusion can be established with thrombolytic agents. Furthermore, the differential treatment effect in the setting of comparable ischemic insults implies that different modifiable biochemical processes may be present during temporary but not permanent focal ischemia, thus providing indirect evidence for reperfusion injury.     

Reproducibility of cerebral cortical infarction in the wistar rat after middle cerebral artery occlusion

Although middle cerebral artery (MCA) occlusion in the rat is often used to study focal cerebral ischemia, the model of ischemia affects the size and reproducibility of infarction. The purpose of this experiment was to methodically examine different preparations to determine the optimum focal cerebral ischemia model to produce a reproducible severe ischemic injury. Eighty-two Wistar rats underwent either 1 hour, 3 hour, or permanent MCA occlusion combined with no, unilateral, or bilateral common carotid artery artery (CCA) occlusion. Three days after ischemia, the animals were prepared for tetrazolium chloride assessment of infarction size. One-hour MCA occlusion produced a coefficient of variation (CV) of 200% with an infarction volume of 20.3+/-10.5 mm(3). Adding unilateral or bilateral CCA occlusion resulted in a CV of 134% and 101%, respectively. Three-hour MCA occlusion combined with bilateral CCA occlusion decreased the CV to 58% with a cortical infarction volume of 82.6+/-12.1 mm(3), P<05, compared with 1-hour MCA occlusion with or without CCA occlusion. Permanent MCA occlusion combined with 3 hours of bilateral CCA occlusion resulted in a CV of 47% with a cortical infarction volume of 89.6+/-16.0 mm(3). These results indicate that 3-hour MCA occlusion combined with bilateral CCA occlusion provide consistently a large infarction volume after temporary focal cerebral ischemia.     

Neurological deficit and cerebral infarction after temporary middle cerebral artery occlusion in unanesthetized cats

Forty-four unanesthetized cats underwent temporary middle cerebral artery (MCA) occlusion with an implanted, externally controlled balloon cuff occluder. The occlusion was reversed to allow reperfusion of the MCA after 2 min to 24 hr of ischemia. Fourteen cats had temporary occlusions lasting 2 min to 3 hr; their neurological deficits improved or resolved after reperfusion, and brain sections showed only scattered microscopic areas of necrosis. After a 4-hr occlusion, five of nine cats (55%) recovered completely within 24 hr; two had persistent deficit when sacrificed, 10 days later, and each had a circumscribed infarct. All 18 cats undergoing 5-, 6-, 8-, and 24-hr occlusions sustained permanent neurological deficits. Three 3-hr occlusions at 2-day intervals in three cats resulted in permanent deficits and infarcts that were 25% larger than those after single 8-hr occlusions. Ten cats underwent permanent MCA occlusion; three deteriorated neurologically and died, and the survivors showed no improvement. Infarcts after 5-, 6-, and 8-hr occlusions followed by reperfusion were 66% smaller (p less than 0.05) than those after permanent occlusion; reperfusion after 24 hr of occlusion did not reduce infarct size. Hemorrhagic infarction occurred after two permanent occlusions, but after only one 5-hr temporary occlusion. The results obtained with this method of temporary regional ischemia indicate that restoration of flow after 1-8 hr, but not after 24 hr, of MCA occlusion resulted in less severe neurological deficit and smaller infarcts than did permanent occlusion. The infarct size correlated with the duration of MCA occlusion (p less than 0.05) rather than with the degree of deficit during occlusion.     

Hypothermic protection in rat focal ischemia models: strain differences and relevance to "reperfusion injury".

Hypothermic protection was compared in Long-Evans and spontaneously hypertensive rat (SHR) strains using transient focal ischemia, and in Wistar and SHR strains using permanent focal ischemia. Focal ischemia was produced by distal surgical occlusion of the middle cerebral artery and tandem occlusion of the ipsilateral common carotid artery (MCA/CCAO). Moderate hypothermia of 2 hours' duration was produced by systemic cooling to 32 degrees C, with further cooling of the brain achieved by reducing to 30 degrees C the temperature of the saline drip superfusing the exposed occlusion site. Infarct volume was determined from serial hematoxylin and eosin-stained frozen sections obtained routinely at 24 hours, or in some cases after 3 days' survival. In the SHR, moderate hypothermia was only effective when initiated before recirculation after a 90-minute occlusion period. In contrast, the same intervention was strikingly effective in the Long-Evans rat even when initiated after as long as 30-minute reperfusion after a 3-hour occlusion. This magnitude and duration of cooling was not protective in permanent MCA/CCAO in the SHR, but such transient hypothermia did effectively reduce infarct volume after permanent occlusions in Wistar rats. These results show striking differences in the temporal window for hypothermic protection among rat focal ischemia models. As expected, "reperfusion injury" in the Long-Evans strain is particularly responsive to delayed cooling. The finding that the SHR can be protected by hypothermia initiated immediately before recirculation suggests a rapidly evolving component of injury occurs subsequent to reperfusion in this model as well. Hypothermic protection after permanent occlusion in Wistar rats identifies a transient, temperature-sensitive phase of infarct evolution that is not evident in the unreperfused SHR. These observations confirm that distinct mechanisms can underlie the temporal progression of injury in rat stroke models, and emphasize the critical importance of considering model and strain differences in extrapolating results of hypothermic protection studies in animals to the design of interventions in clinical stroke.     

大鼠脑缺血再灌注后MMP-9的表达及人工合成E-选择素的干预作用

目的：研究肿瘤坏死因子-α（TNF-α）和基质金属蛋白酶-9（MMP-9）参与大鼠脑缺血再灌注损伤的机制及人工合成E-选择素保护作用的机制。方法：健康SD大鼠,随机分为手术组、假手术组和治疗组。手术组建立大鼠局灶性脑缺血再灌注损伤模型;治疗组术前从股静脉注射人工合成E-选择素;假手术组仅将线栓插到颈外动脉、颈内动脉分叉处,其余步骤同手术组。免疫组化检测脑组织中TNF-α和MMP-9的表达,RT-PCR检测MMP-9mRNA的表达。结果：手术组TNF-α、MMP-9和MMP-9mRNA表达与假手术组比较均有明显升高（P〈0．05）;治疗组TNF-α、MMP-9和MMP-9mRNA表达水平比手术组明显下降（P〈0．05）。相关分析表明,MMP-9mRNA分别与TNF-α和MMP-9的表达呈正相关。结论：大鼠脑缺血再灌注后TNF-α能够在转录水平诱导MMP-9的表达。人工合成E-选择素降低大鼠脑缺血再灌注后缺血脑组织MMP-9表达的机制可能是抑制TNF-α对MMP-9mRNA合成的诱导,从而降低了MMP-9的表达。     

神经节苷脂对大鼠脑缺血再灌注损伤的脑保护作用

目的探讨神经节苷脂对大鼠脑缺血再灌注损伤的脑保护作用。方法采用线栓法制作缺血再灌注大鼠模型,分别用神经节苷脂(治疗组)和生理盐水(对照组)腹腔注射。观察两组大鼠缺血90min、缺血90min再灌注24h的脑梗死面积、神经功能缺损程度、细胞凋亡数、细胞凋亡率。结果治疗组大鼠于相同时间点脑梗死面积较对照组明显减小,仅表现轻度的神经功能缺损,且神经细胞的凋亡数较对照组显著减少(均P<0.01)。结论神经节苷脂能明显减小大鼠实验性脑缺血的脑梗死面积,减轻脑缺血再灌注后神经功能缺损程度,显著减轻缺血区神经元损害,具有显著的脑保护作用。     

Cortical infarct volume is dependent on the ischemic reduction of perifocal cerebral blood flow in a three-vessel intraluminal MCA occlusion/reperfusion model in the rat

Occlusion of the middle cerebral artery (MCA) causes a reduction of cerebral blood flow (CBF), which shows a progressive decrease from the periphery to the core of the MCA territory. The severity of ischemia is dependent on the duration of the ischemic episode and degree of CBF reduction. Fixing the ischemic episode to 1 h, we have examined whether or not cortical infarct size was related to the degree of CBF reduction in a perifocal cortical area in rats. One-hour intraluminal MCA occlusion accompanied with bilateral common carotid artery (CCA) occlusion (three-vessel occlusion/reperfusion model) was carried out in Sprague-Dawley rats and CBF was monitored with laser-Doppler flowmetry in the fronto-parietal cortex, an area which is perifocal to the core of the MCA territory. Finally, infarct size was measured 7 days later and was related to the corresponding CBF decrease. Sequential ipsilateral CCA, MCA and contralateral CCA occlusions produced reductions of CBF to 96%, 52% and 33% of baseline, respectively. Cortical infarct volume was found to be dependent on the corresponding reduction of perifocal cortical CBF during the ischemic episode. These results show that the reduction of CBF in the periphery of the MCA territory during 1-h focal ischemia determines infarct size in a three-vessel occlusion/reperfusion model.     

高同型半胱氨酸血症对脑缺血再灌注损伤影响的实验研究

目的：探讨高同型半胱氨酸血症（HHcy）对脑缺血再灌注损伤的影响。方法：制备HHcy大鼠大脑中动脉缺血再灌注损伤模型，检测缺血l、2和4h再灌注24h不同时间窗各组大鼠脑梗死体积及血浆总同型半胱氨酸（tHcy）、超氧化物歧化酶（SOD）和丙二醛（MDA）水平。结果：HHcy组大鼠脑缺血再灌注不同时间窗各组分别较相应对照组脑梗死体积增加，SOD水平降低，MDA水平增高，差异均有统计学意义（均P〈0．05）；HHcy组和对照组大鼠脑缺血再灌注不同时间窗各组脑梗死体积的差值随缺血时间的延长而增加（均P〈0．05），但SOD与MDA水平的差值各组间无统计学意义（均P〉0.05）。结论：HHcy可能通过促进氧自由基产生等作用加重脑缺血再灌注损伤。     

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.