Enhanced arteriogenesis for prevention of ischemic brain damage

将原有的新生侧支动脉正向外向重塑为功能性传导动脉，即动脉生成，是预防卒中后缺血性损伤的主要内源性抢救机制。本实验采用实验性慢性脑低灌注小鼠模型，观察碱性成纤维细胞生长因子-2促进脑动脉新生的作用机制及对缺血性脑损伤的影响。脑低灌流显著增加小鼠脑内软脑膜动脉的管径，增加血管内皮细胞或平滑肌细胞的数量。低灌注组或假手术组动物随后行同侧大脑中动脉闭塞，并评估脑梗塞体积。低灌流组小鼠的总梗塞体积明显小于假手术组。应用成纤维细胞生长因子-2促进侧支动脉生长，进一步减少梗塞体积，导致长期的功能恢复。

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.