兔短暂性局灶脑缺血MRI动态演变和病理组织学改变

目的：研究兔短暂局灶脑缺血后MRI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：30只新西兰白兔分为7min和30min短暂大脑中动脉阻塞模型和假手术组，各组10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，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异常。在7min和30min组，在阻塞时的DWI高信号于再灌注后消失。此后，在7min组，DWI和T2WI保持正常，而在30min组，于6～12h观察点出现继发的DWI高信号和T2WI异常。组织学检查显示在2组均有神经元坏死，但是坏死神经元数目在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，以及有些经历过短暂性脑缺血发作的患者表现认知功能改变。

Ischemic lesions on MRI and histological outcomes after different transient periods of focal ischemia in rabbits

Objective： To investigate the time course of ischemic changes on MRI（including DWI and T2WI） after different brief periods of focal brain isehemia in rabbits and to evaluate the histopathological outcomes in the regions of DWI abnormalities, Methods： Thirty rabbits were subjected to 7 minutes（n=10）; 30 minutes（n=10） short time obliteration of middle cerebral arterial occlusion and sham operation（n=10）. MRI（including DWI and T2WI） were performed during and before occlusion; 5min after occlusion and at 0.5, 2, 6, 12, 24, 48 and 72 hours of reperfusion. After the last MRI study at 72 hours of reperfusion, the brains were evaluated by histopathology. Results： No MRI abnormalities were observed in the sham-operated rabbits. In the 7-minute and 30-minute groups, the perfusion deficits and DWI hyperintensities that occurred during occlusion disappeared shortly after reperfusion. The DWI and T2WI results remained normal in the 7-minute group, whereas secondary DWI hyperintensity and T2WI abnormalities developed at the 6-12 hour observation point in the 30-minute group. Histological examinations demonstrated neuronal necrosis in the two groups, but the number of necrotic neurons was significantly higher in the 30-minute group than in the 7-minute group （P〈0.001）. Conclusions： Transient or permanent resolution of initial DWI lesions after repcrfusion depends on the duration of isehemia. Transient resolution of DWI lesions was associated with widespread neuronal necrosis; moreover, permanent resolution of DWI lesions did not necessarily indicate complete salvage of brain tissue from ischemic injury. These results may help to explain the neurological deficits in some patients who have normal DWI results after cerebral ischemia and cognitive deficits in some patients who experienced transient ischemic attacks.