内皮细胞一直被认为是影响微血管血流的靶点，而新近的研究表明，Pericyte（周细胞）在调控脑、视网膜及肿瘤微血管血流中起更重要的作用，但其在心脏微血管中的作用及调控机制尚不清楚。前期工作中我们发现炎症因子在介导平滑肌细胞收缩中起重要作用，由此我们推测心肌缺血再灌注后炎症因子释放可能介导微血管上的具有平滑肌细胞收缩特性的周细胞收缩，调控血流。本研究拟通过对GFP转基因小鼠心脏微血管周细胞及内皮细胞单独培养和联合培养，结合我们前期工作中的"活体冷冻技术"，分别从细胞水平、分子水平和组织水平探讨心肌缺血再灌注后炎症因子释放可能改变周细胞与内皮细胞间Cx43表达，进而改变内皮细胞PDGFB分泌及其受体PDGFRβ在周细胞表达，最终引发周细胞钙离子内流而收缩，影响血流。以周细胞和内皮细胞作为共同治疗靶点来调控血流的抗肿瘤治疗已表明具有更好的疗效，因此，周细胞引入为心肌缺血再灌注治疗提供新靶点。

Endothelial cells has been considered the sites of regulating microvascular blood, but recent studies show that, Pericyte act a more prominent role in the regulation of microvascular blood flow of brain, retina or tumor. Until now, the morphological distribution of Pericyte and its effect on microvascular regulation mechanism is not clear in the cardiac microvasculature. In previous work we found that inflammatory cytokines plays an important role in mediating contraction of smooth muscle cells, on which we speculate that the release of inflammatory factors induced by myocardial ischemia reperfusion injury may mediate the contraction of Pericyte containing smooth muscle cell contraction characteristics, regulation of blood flow. In the present study, Pericytes and endothelial cells derived from GFP transgenic mouse heart will be cultured alone or combination. With applying our earlier work of the" in vivo cryotechnique", the mechanism will be surveyed in the cellular level, molecular level and histological level that inflammatory factors induced by myocardial ischemia reperfusion may change the Pericytes and endothelial cell Cx43 expression, changes the secretion of PDGFB from endothelial cells and its receptor PDGFR beta expression in Pericytes, trigger Pericytes calcium influx, contracting and effecting blood flow. Anti-tumor therapy aimed endothelial cells and Pericytes as the combination therapeutic targets have been shown to have better curative effect. This study introduces Pericytes the new ideas and new targeted for myocardial ischemia reperfusion therapies.