Cerebral venous infarction (CVI) caused by the injury of cortical bridging veins (CBVs), is one of the most serious complications following neurosurgical craniotomy. Different from cerebral artery infarction, this CVI pathological process is more complicated, accompanied by acute venous hypertension, brain edema, cerebral ischemia and hemorrhage in the veins bridged brain area. Therefore, a reliable and stable small animal model is particularly important for the pathological study of CVI induced by surgical CBV interruption (CBVi). A mouse model established by cutting off the right CBVs from bregma to lambda with microsurgical technique is used for the assessment of the pathological process. Adult male mice underwent craniotomy after transection of the parietal skin under anesthesia. The right CBVs were exposed by removing the right skull along the right lateral edge of the sagittal sinus (forming a 4 mm × 3 mm bone window from bregma to lambda) with a drill under the operating microscope. Following the final inspection of the cerebral veins, the CBVs (30% one, 60% two, 10% none) were sacrificed using bipolar coagulation technique. Intracranial pressure (ICP) monitoring, motor function examination, brain edema assessment and brain histopathological observation after perfusion were performed at different time points (6 h, 12 h, 24 h, and 48 h) in the postoperative mice. Cerebral hemisphere swelling, midline shift and subcortical petechial hemorrhage were found on histological sections 6 h after CBVs dissection. The change of ICP was consistent with cerebral edema and peaked at 12 h after surgery, as well as the disruption of the blood-brain barrier assessed by Evans Blue staining. Tissue necrosis, nerve cell loss and monocytes infiltration were also dynamically increased in the postoperative hemispheric cortex. Behavioral tests showed obvious somato- and forelimb-motor dysfunction, and severe somatosensory disorder on the operative mice at 12 h, which were substantially recovered at 48 h. Our study provided a novel mouse model of CVI caused by surgical CBVi that was close to clinical practice, and preliminarily confirmed its pathological process. This model might become an important tool to study the clinical pathology and the molecular mechanism of nerve injury following CVI.

中文翻译：

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小鼠皮层桥静脉手术中断致脑静脉梗死后脑损伤的特点.

由皮质桥静脉 (CBV) 损伤引起的脑静脉梗塞 (CVI) 是神经外科开颅手术后最严重的并发症之一。与脑动脉梗死不同，这种CVI的病理过程更为复杂，伴有急性静脉高压、脑水肿、脑缺血和脑桥区静脉出血。因此，一个可靠、稳定的小动物模型对于手术CBV中断（CBVi）诱发的CVI的病理学研究尤为重要。通过使用显微外科技术切断从前囟到 lambda 的正确 CBV 建立的小鼠模型用于评估病理过程。成年雄性小鼠在麻醉下横切顶叶皮肤后进行开颅手术。通过在手术显微镜下用钻头沿着矢状窦右侧边缘（从前囟到 lambda 形成一个 4 mm × 3 mm 的骨窗）去除右侧颅骨，暴露右侧 CBV。在对脑静脉进行最终检查后，使用双极凝固技术处死 CBV（30% 1，60% 2，10% 无）。在不同时间点（6 h、12 h、24 h和48 h）对术后小鼠进行颅内压（ICP）监测、运动功能检查、脑水肿评估和灌注后脑组织病理学观察。CBVs解剖后6小时在组织切片上发现大脑半球肿胀、中线移位和皮层下点状出血。ICP 的变化与脑水肿一致，在术后 12 h 达到峰值，以及通过伊文思蓝染色评估的血脑屏障的破坏。术后半球皮质中的组织坏死、神经细胞丢失和单核细胞浸润也动态增加。行为测试显示，手术小鼠在12小时时出现明显的躯体和前肢运动功能障碍，以及严重的体感障碍，并在48小时时基本恢复。我们的研究提供了一种接近临床实践的由手术CBVi引起的CVI的新型小鼠模型，并初步证实了其病理过程。该模型可能成为研究 CVI 后神经损伤的临床病理和分子机制的重要工具。术后半球皮质中的神经细胞损失和单核细胞浸润也动态增加。行为测试显示，手术小鼠在12小时时出现明显的躯体和前肢运动功能障碍，以及严重的体感障碍，并在48小时时基本恢复。我们的研究提供了一种接近临床实践的由手术CBVi引起的CVI的新型小鼠模型，并初步证实了其病理过程。该模型可能成为研究 CVI 后神经损伤的临床病理和分子机制的重要工具。术后半球皮质中的神经细胞损失和单核细胞浸润也动态增加。行为测试显示，手术小鼠在12小时时出现明显的躯体和前肢运动功能障碍，以及严重的体感障碍，并在48小时时基本恢复。我们的研究提供了一种接近临床实践的由手术CBVi引起的CVI的新型小鼠模型，并初步证实了其病理过程。该模型可能成为研究 CVI 后神经损伤的临床病理和分子机制的重要工具。我们的研究提供了一种接近临床实践的由手术CBVi引起的CVI的新型小鼠模型，并初步证实了其病理过程。该模型可能成为研究 CVI 后神经损伤的临床病理和分子机制的重要工具。我们的研究提供了一种接近临床实践的由手术CBVi引起的CVI的新型小鼠模型，并初步证实了其病理过程。该模型可能成为研究 CVI 后神经损伤的临床病理和分子机制的重要工具。