The circulating nitric oxide pool and anemia in acute myocardial infarction (B06)

作为急性心肌梗死死亡率增加原因的贫血的潜在机制在很大程度上尚不清楚。在之前的资助阶段，我们发现红细胞(RBC)通过活跃的eNOS依赖的信号通路为循环中的一氧化氮(NO)池做出贡献。在我们的实验模型中，贫血导致RBC功能障碍，eNOS依赖的心脏和循环功能代偿，并增加急性心肌梗死的死亡率。现在，我们希望将这些实验结果转化为临床研究。总的假设是血管内皮细胞和红细胞功能障碍导致再灌流急性心肌梗死急性期贫血的不良反应。

The underlying mechanisms of anemia as cause of increased mortality in AMI is largely unidentified. In the previous funding period, we showed that red blood cells (RBC) contribute to the circulating nitric oxide (NO) pool through an active eNOS-dependent signaling pathway. In our experimental models anemia causes RBC dysfunction, eNOS-dependent cardiac and circulatory functional compensation, and increased mortality from AMI. Now, we would like to transfer these experimental findings into clinical studies. The overall hypothesis is that endothelial and RBC dysfunction contributes to the adverse effects of anemia in the acute phase of reperfused AMI.