减阻剂对冠脉再通后心肌无复流现象的影响及机制

项目名称： 减阻剂对冠脉再通后心肌无复流现象的影响及机制

项目编号： No.81200144

项目类型： 青年科学基金项目

立项/批准年度： 2013

项目学科： 医学一处

项目作者： 胡锋

作者单位： 扬州大学

项目金额： 23万元

中文摘要： 经皮冠脉介入治疗开通闭塞冠脉后，部分患者的缺血区心肌组织微循环血流缓慢甚至无血流灌注，这一现象被称为心肌无复流现象。目前针对心肌无复流现象的治疗尚无成熟的方法。减阻剂是一类可以降低流体阻力作用的高分子聚合物。近来我们观察到,减阻剂可以明显增加大鼠大动脉、微小动脉及毛细血管网的血流速度及减低血流阻力，也可有效地减少急性心梗大鼠的梗死面积，显著增强心功能,增加心梗后存活率。据此，我们推测：减阻剂可以通过减低冠状动脉及微循环血流阻力，增加冠脉血供，改善冠脉再通后心肌无复流现象。本研究使用心肌声学造影、血流动力学检测、组织病理学检测等不同方法，探讨急性心肌梗死后冠脉开通时减阻剂对心肌微循环的影响，并在缺血再灌注损伤、分子生物学等层面探讨其机制。首次通过整体、器官、组织形态、分子等多个层面深入探讨减阻剂对冠脉再通后心肌无复流现象的可能影响及其机制。为PCI术后心肌无复流现象的防治提供新的治疗思路。

中文关键词： 减阻剂；无复流现象；急性心肌梗死；心肌声学造影；心肌灌注

英文摘要： Myocardial no-reflow phenomenon known as myocardial tissue perfusion does not occur after the occluded coronary artery have been re-opened by percutaneous coronary intervention (PCI). There are no effective methods or medicine to treat myocardial no-reflow until now. Drag-reducing polymers (DRPs) are blood-soluble macromolecules that can increase blood flow and reduce vascular resistance. A number of our early studies have found that DRPs can increase blood flow and reduce blood resistance of aorta, small arteries and capillary of rat. DRPs also can reduce myocardial infarct size in acute myocardial infarction in rats, increase survival rate and improve heart function in rats with myocardial infarction. Accordingly, we hypothesized that DRPs can reduce the resistance of coronary arteries and myocardial microcirculation, increase coronary artery blood supply, reduce myocardial no-reflow phenomenon after coronary artery recanalization. Myocardial contrast echocardiography, hemodynamic monitor, histopathology, molecular biological test and many other technologies are chose in this study. This is the first time to explore the effect and mechanism of DRPs on myocardial no-reflow phenomenon through multiple levels. DRPs may offer a new potential approach for the treatment of myocardial no-reflow phenomenon after PCI.

英文关键词： drag-reducing polymers；no-reflow phenomenon；acute myocardial infarction；myocardial contrast echocardiography；myocardial perfusion