Abstract
Objective: Embolic occlusion of the middle cerebral artery (MCA) leads to distal perfusion deficits as the vessel is recanalized. However, the mechanism for the perfusion deficits is not fully understood. The authors examined whether distal movement of fragments formed from the original thrombus contributes to the perfusion deficits.
Methods: In the first series, they studied whether the reduction in perfusion deficits is due to the dissolution of the original clots embolized or due to collateral perfusion. In the second series, they studied whether fragments formed from the original clots move to distal arterial system. In the third series, they studied whether plasmingen activator plays a role in the thrombolysis following ischemia.
Results: Occlusion of MCA permanently resulted in large perfusion deficits in the ipsilateral hemisphere, and these perfusion deficits did not change significantly after the occlusion. In contrast, perfusion deficits reduced significantly in a model of transient MCA occlusion. The numbers of fragments formed from the original clots increased gradually after the MCA occlusion in the ischemic injured brain. In addition, expression of urokinase plasminogen activator was also upregulated.
Conclusion: The present study thus reveals the mechanisms of the downstream arterial occlusion following the dissolution of original thrombus.
This work is supported by Canadian Institute of Health Research and Heart and Stroke Foundation of Canada (AS and CXW).