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T3 improves left ventricular function in a rodent model with a myocardial infarction
Author(s) -
Henderson Kyle K,
Danzi Sara,
Klein Irwin,
Samarel Allen M
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.742.9
Subject(s) - medicine , cardiology , contractility , myocardial infarction , ejection fraction , heart failure , serca , ligation , cardiac function curve , infarction , endoplasmic reticulum , endocrinology , atpase , chemistry , biochemistry , enzyme
Serum triiodothyronine (T3) concentration is reduced in patients with congestive heart failure which may contribute to the altered expression of thyroid hormoneresponsive genes. We hypothesize that T3 supplementation in a rat model of left ventricular (LV) dysfunction will increase α/β myosin heavy chain (MHC) ratio, sarco/endoplasmic reticulum Ca 2+ ATPase (SERCA) expression, and thereby improve LV function. Echocardiography was used to assess LV structure and function in male Sprague Dawley rats (~300g), before and after left anterior descending coronary artery ligation. One week post‐ligation, LV function was significantly attenuated; ejection fraction was reduced from 38±1% to 21±1%. Saline control or T3 supplementation was then started at 3, 6 and 60μg/kg/day for 8wks. Radiotelemetry was used to measure body temperature, ECG, and arterial blood pressure in a subset of animals. LV structure and function, at 2, 4, 6 and 8wks were not changed by T3 supplementation as measured by echocardiography. However, LV catheterization at 8wks demonstrated that animals receiving T3 supplementation at 6 or 60μg/kg/day had significantly greater LV contractility (+dP/dt) and a trend toward improved LV relaxation (Tau). LV RNA was extracted for measurement of α and β MHC and SERCA mRNA. These findings support the hypothesis that T3 supplementation may improve the function of the remaining viable LV tissue in rats with a myocardial infarction. Funding: Ralph and Marian Falk Medical Research Trust and King Pharmaceuticals.