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

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.

DFG Programme Collaborative Research Centres

Subproject of SFB 1116:  Master switches in cardiac ischemia

Major Instrumentation ENO-30 mit Autosampler- für die Messung von NO metaboliten im Plasma und Geweben (wie in WP1 und WP2 beschrieben)

Instrumentation Group 1350 Flüssigkeits-Chromatographen (außer Aminosäureanalysatoren 317), Ionenaustauscher

Applicant Institution Heinrich-Heine-Universität Düsseldorf

Project Heads Professorin Dr. Miriam Margherita Cortese-Krott, until 12/2018; Professor Dr. Christian Jung; Professor Dr. Malte Kelm