|
Iron deficiency (ID) induces cardiac and neural alterations, such as cardiac hypertrophy and apoptosis, electron transport dysfunction, and brain mitochondrial disruption. Cardiac norepinephrine (NE) depletion suggests chronically high sympathetic nervous system (SNS) traffic to the heart. Thus, ID would be expected to affect heart function and blood pressure, and our previous experiments have shown baroreflex alterations after 4 weeks of ID. HYPOTHESES (1) Chronic high SNS output initially leads to a hyperfunctional heart with higher left ventricular pressure (LVP) and heart rates (HR) at each mean arterial pressure (MAP), and (2) eventual depletion of NE, along with heart apoptosis and debility, is coincident with reduced LVP and HR at all MAP. METHODS Rats were fed control (CN) or ID diets for 2 or 4 weeks. Baroreflex experiments were conducted using ramp (before and after atropine) and steady state protocols. Hearts were excised for Langendorff experiments to obtain LVP at set flow rates. RESULTS Hematocrit verified ID (p ≤ 0.05); heart mass verified hypertrophy. Baroreflex preliminary data suggests higher HR at all MAP at 2 weeks, but lower HR after 4 weeks; experiments continue at time of writing. Langendorff data indicates higher LVP with ID at 2 weeks, but lower LVP after 4 weeks. CONCLUSION Changes with ID are adaptive at 2 weeks but pathological after 4 weeks. Supported by WY INBRE (LC4090).
|
