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

贫血作为AMI死亡率增加的原因的潜在机制在很大程度上尚未确定。在上一个资助期，我们发现红细胞（RBC）通过一个活跃的eNOS依赖性信号通路促进循环一氧化氮（NO）库。在我们的实验模型中，贫血导致RBC功能障碍、eNOS依赖性心脏和循环功能补偿以及AMI死亡率增加。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，内皮细胞和红细胞功能障碍有助于在急性再灌注心肌梗死贫血的不利影响。

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.