超急性期溶栓治疗被认为是治疗急性脑梗死的有效方法。但部分患者溶栓治疗后，即使栓塞部位血流恢复，其近远期临床转归仍不理想。究其机制，可能与血管栓塞后微血管血栓形成有关。目前，部分研究提出颅内大血管栓塞后微血管血栓形成可能与CD40-CD40L信号通路有关。但仍存在一些问题：1）模型建立采用线栓法或光化学法，而人脑梗死是自体血栓栓塞，两者在发病机制上存在差别。2）既往研究多选用大鼠作实验对象，大鼠与人在神经体液调节方面差别较大。3）既往研究未能阐述CD40-CD40L信号通路在颅内微血管血栓形成过程中的具体机制。因此，本实验在成功建立犬脑梗死模型的基础上，拟研究：1）颅内大血管栓塞后微血管血栓形成量的时间变化规律。2）观察CD40-CD40L信号通路下游细胞因子的变化，并联合多模态MRI，阐述其调控微血管血栓形成的可能机制。同时采用通道抑制剂反证该信号通道的调控作用，具有重要的理论意义。

Thrombolytic therapy is the only proven effective treatment for superacute ischemic stroke. However, part of the patients could not recover ideally, even the occluded vessel had been recanalized. Microvascular thrombosis followed after cerebral artery occlusion was deemed to be responsible for the unsatisfactory clinical outcome. Recent years, several studies indicated the CD40/CD40L signal pathway might result in the microvascular thrombosis. However, previous related studies have several problems. Firstly, the ischemic models were established using thread embolization or photochemical method. However, the human ischemic events were mostly due to the autogenous clot embolization. Secondly, most of the previous studies used the rats as the experiment animals. However, there were significant difference between the rats and human regarding the neurophysiology. Thirdly, previous studies did not clarify the potential exact mechanism regarding that how the CD40/CD40L signal pathway regulated the formation of the microvascular thrombosis. Therefore, base on our previous beagle dogs cerebral ischemic model established using intervention technique and autogenous clot , we try to evaluate the time course regarding the formation of microvascular thrombosis, clarify the potential mechanism regarding that how the CD40/CD40L signal pathway regulated the formation of the microvascular thrombosis via monitoring the temporal change of downstream cytokine and the multimodal MR methods. Meanwhile, we would use the signal pathway inhibitor to furnish counterevidence regarding CD40/CD40L signal pathway regulated the formation of the microvascular thrombosis. Finally, this study would provide theoretical basis for using the CD40/CD40L signal pathway related drugs to reduce the formation of the microvascular thrombosis and improve the clinical outcome of ischemic events after thrombolytic therapy.