Department

Biology Department

First Advisor

Dr. Bud Chew

Description

Cardiac hypertrophy, enlargement of the heart, can be adaptive or pathological. Athletes increase cardiac output and ventricular chamber size; congestive heart failure decreases cardiac output without chamber enlargement. Iron deficiency causes cardiac hypertrophy through sympathetic stimulation, but its physiology is unknown. We believe iron deficient hypertrophy begins as adaptiv e, but transitions to pathological. We hypothesized that four weeks of iron deficiency would result in failing cardiac function and decreased sympathetic neurotransmitter stores. We placed rats on a four - week iron deficient diet, then determined cardiac fu nction in vivo using pressure - volume loops. We implanted catheters in both femoral veins (for drug infusion), a jugular vein (for saline calibration), and inserted a pressure - volume micro - catheter into the left ventricle via the right carotid artery. We oc cluded the inferior vena cava for load - independent measurement of contractility, and infused hypertonic saline via jugular vein for parallel conductance calibration. We used dopamine (beta - agonist) and atenolol (beta - antagonist) to assess activation and de activation of the sympathetic nervous system, respectively. We heparinized and decapitated rats; collected blood for cuvette calibration (for conductance - volume calibration), hematocrits, and plasma catecholamine analysis by HPLC. We dissected hearts for morphometric and HPLC analysis. At abstract submission, data collection is complete, and analysis is underway.

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Physiology of Cardiac Hypertrophy in Severely Iron Deficient Rats Using Pressure - Volume Loops

Cardiac hypertrophy, enlargement of the heart, can be adaptive or pathological. Athletes increase cardiac output and ventricular chamber size; congestive heart failure decreases cardiac output without chamber enlargement. Iron deficiency causes cardiac hypertrophy through sympathetic stimulation, but its physiology is unknown. We believe iron deficient hypertrophy begins as adaptiv e, but transitions to pathological. We hypothesized that four weeks of iron deficiency would result in failing cardiac function and decreased sympathetic neurotransmitter stores. We placed rats on a four - week iron deficient diet, then determined cardiac fu nction in vivo using pressure - volume loops. We implanted catheters in both femoral veins (for drug infusion), a jugular vein (for saline calibration), and inserted a pressure - volume micro - catheter into the left ventricle via the right carotid artery. We oc cluded the inferior vena cava for load - independent measurement of contractility, and infused hypertonic saline via jugular vein for parallel conductance calibration. We used dopamine (beta - agonist) and atenolol (beta - antagonist) to assess activation and de activation of the sympathetic nervous system, respectively. We heparinized and decapitated rats; collected blood for cuvette calibration (for conductance - volume calibration), hematocrits, and plasma catecholamine analysis by HPLC. We dissected hearts for morphometric and HPLC analysis. At abstract submission, data collection is complete, and analysis is underway.