Enhanced arteriogenesis for prevention of ischemic brain damage

预先存在的De-novo侧支动脉向功能性传导动脉的正性向外重塑，即动脉生成，是预防卒中后缺血性损伤的主要内源性补救机制。在实验性慢性脑低灌注小鼠模型上，应用碱性成纤维细胞生长因子2（basic fibroblast growth factor 2，FGF-2）促进动脉生成，以探讨动脉生成的机制或对缺血性脑损伤的影响。低灌注或假手术动物随后进行同侧大脑中动脉闭塞，并评估梗死体积。与假手术组相比，低灌注组小鼠的总梗死体积显著减少。FGF-2给药促进侧支动脉生长，进一步减少梗死体积，导致长期功能恢复。

Positive outward remodeling of pre-existing of De-novo collateral arteries into functional conductance arteries, arteriogenesis, is a major endogenous rescue mechanism to prevent ischemic damage after stroke. We, here, investigated the mechanism of arteriogenesis or examined effect on ischemia brain damage by means of promoting arteriogenesis with basic fibroblast growth factor 2 (FGF-2) in experimental chronic brain hypoperfused mice model.Brain hypoperfusion significantly increased the diameter of leptomeningeal arteries,and the number of proliferating endothelial or smooth muscle cells in the arteries. Hypoperfused or sham animals underwent subsequent ipsilateral middle cerebral artery occlusion, and infarct volume was assessed. The total infarction volume was significantly decreased in hypoperfused mice than sham-operated animals. FGF-2 administration enhanced collateral artery growth and further reduced infarction volume, resulting in long-term functional recovery.