Iron deficiency alters Langendorff heart function

Iron deficiency (ID) causes cardiac hypertrophy and myocyte apoptosis (Dong et. al. 2005). The objective of this study was to determine whether iron deficient (ID) hearts function normally in an isolated Langendorff preparation, before and after norepinephrine (NE) perfusion. CD rats (Harlan) were put on an ID or control (C) diet for 4 weeks; ID was confirmed by microhematocrit (p<0.05). Hearts were removed from anesthetized (Ketaset) rats and quickly put on the Langendorff apparatus (PowerLab, AD Instruments). An oxygenated physiological salt solution with glucose (PSS; pH=7.4) perfused the heart; temperature was constant. A balloon catheter was inserted through the left atrium into the left ventricle (LV) for continual LV pressure measurement. With constant PSS flow at 5 ml/min, ID hearts had a significantly lower heart rate (HR; p<0.0001) and a trend for lower pulse pressure (PP; p=0.0536). When perfused with PSS with norepinephrine (NE), ID hearts had increased HR and PP when compared to C (p<0.0001). Hearts were then returned to PSS perfusion for several minutes, after which, we increased flow in a stepwise manner to determine whether ID and C hearts followed the Frank‐Starling relationship. PP was used as an index of force generation by the LV myocardium. C hearts adhered closely to the Frank‐Starling relationship (R‐squared = 0.92; p<0.0001); ID hearts did not (R‐squared = 0.284; p<0.0001). Further, the slope of the PP vs. flow line was significantly lower for ID than C (alpha<0.05). We conclude that ID hearts are hypersensitive to NE, and do not adhere to the Frank‐Starling relationship. Supported by the Wyoming NIH INBRE Grant (LC4090).