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2009 Southern Regional Meeting Abstracts
Session: Joint Plenary Poster Session and Reception
ECHOCARDIOGRAPHY REVEALS PROGRESSIVE CARDIAC DYSFUNCTION IN Mg-DEFICIENT RATS
Kramer JH1, Spurney C3, Mak I1, Iantorno M3, Tziros C2, Weglicki WB1,2. 1The George Washington University Medical Center, Washington, D.C., DC; 2The George Washington University Medical Center, Washington, D.C., DC and 3Children's National Medical Center, Washington, D.C., DC.
Purpose of Study: The impact of chronic dietary Mg-deficiency on in situ cardiac function in rats was investigated using non-invasive echocardiography (EC).
Methods Used: Male Sprague-Dawley (180g) rats were placed on Mg-deficient (MgD, 9% RDA) or Mg-sufficient (MgS, 100% RDA) diets for 3 or 5 weeks. EC was performed at 3 and 5 wks, and blood samples collected for assessment of substance P (SP by ELISA), and oxidative stress indices (RBC glutathione loss, isoprostane production and neutrophil basal superoxide production).
Summary of Results: Three wks of MgD failed to induce significant changes in EC parameters (vs MgS), except for a 20% decline (p<0.05) in the mitral valve E/A ratio (E/A), a sign of early diastolic dysfunction. By contrast, 5 wks of MgD led to significant (p<0.05) depression in: LV systolic function (LV ejection fraction [LVEF] by 6.1%; % fractional shortening [%FS] by 16.5%; and maximum aortic pressure [Pmax] by 18.9%); diastolic function [E/A] by 27.7%; and interventricular septum diameter in systole [IVSs] by 18.6%. The cardiac dysfunction at 5 wks was preceded by elevations at 3 wks (and observed at 5 wks) in circulating SP levels (6.5-7.2 fold), RBC glutathione loss (40-45%), plasma isoprostane elevations (50-100%), and higher neutrophil basal superoxide generation (3-5 fold) vs MgS.
Conclusions: The progressive development of oxidative injury during chronic MgD involves neurogenic inflammation due to SP (Exp. Biol. Med. 228:665, 2003). To our knowledge, this is the first echocardiographic demonstration of cardiac dysfunction in an animal model of MgD. Supported by NIH RO1 HL-62282 & HL-65178.
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