急性脊髓损伤（SCI）在原发损伤基础上，出现继发性损伤导致神经元持续坏死、凋亡，严重影响功能恢复。目前SCI继发损伤的机制仍不明确。我们首次在实验中发现：SCI小鼠模型于早期（数分钟）脊髓背侧静脉血管内即出现微血栓。然而既往理论认为在损伤的亚急性期（2-4日）出现组织水肿、血管痉挛和血栓形成进而导致局部血流灌注不足，这与我们所观察到的现象不符。早期微血栓的发生机制及病理和病理生理意义仍未知，我们猜测其可能与内皮细胞损伤、白细胞聚集关系密切，进而加剧继发性损伤导致相应的病理改变。本项目中，我们将通过双光子显微镜、组织透明化成像、微透析等技术研究SCI大鼠模型，进一步观察微血栓形成规律，探索微血栓形成的上游机制以及微血栓形成造成的病理和病理生理结果，并基于此探索干预微血栓形成的方法。本项目为医学和神经生物学的结合，有可能对当前SCI损伤机制的理论做出补充或产生新的认识。

Spinal cord injury (SCI) is an incurable lesion having primary injury as well as secondary injury to induce continuing neurons necrosis and apoptosis. But the secondary injury is still incomprehensible. In our unpublished results we repeatedly found the venous vessels teemed with micro-thrombosis in minutes after SCI in C57BL/6 mice and which is unreported in murine SCI model. The former theory indicates in the subacute phase (2–4 days after injury), further ischaemia occurs owing to ongoing oedema, vessel thrombosis and vasospasm results in sustaining loss of neurons and glia while is contrary to our observation. But neither the mechanism of formation of micro-thrombosis nor its pathological and pathophysiological consequence is still unknown. We presume the acute micro-thrombosis will intensify and worsen the secondary injury connecting to immune reaction and endothelium impairment. In this project we will use 2-photon laser scan microscope, iDISCO+ and microdialysis to research the Sprague-Dawley rat, to survey the mechanism of blood clots formation and its pathological and pathophysiological consequence, and to argue the applicable therapeutic intervene. This study is aiming to get deeper understanding to or get new insight into the formation of microthrombosis and the mechanism of spinal cord secondary injury.