What question did this study set out to answer?

To determine whether thyroxine-induced cardiac hypertrophy stems from systemic circulatory alterations or direct hormonal stimulation of myocardial tissue growth.

April 1, 1966Circulation ResearchOpen Access

Determinants of Thyroxine-Induced Cardiac Hypertrophy in Mice

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To determine whether thyroxine-induced cardiac hypertrophy stems from systemic circulatory alterations or direct hormonal stimulation of myocardial tissue growth.
Administered thyroxine alone or concurrently with reserpine to mice to evaluate hypertrophy while suppressing thyrotoxicosis-associated circulatory changes.
Injected mice with synthetic L-thyroxine and tracked the timing of myocardial protein synthesis in relation to observable changes in systemic circulation.
Mice treated with both reserpine and thyroxine developed cardiac hypertrophy equivalent to mice treated with thyroxine alone, despite significant mitigation of circulatory alterations.
Synthetic L-thyroxine elevated the rate of cardiac protein synthesis prior to the onset of any detectable circulatory changes.

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Implication

May support direct thyroxine effects on myocardium; leaves open relevance to human thyrotoxicosis.

Cite This Study

Cohen et al. (1966) studied this question.

synapsesocial.com/papers/6a70a1beac440176ef294c37 https://doi.org/10.1161/01.res.18.4.388

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Determinants of Thyroxine-Induced Cardiac Hypertrophy in Mice

Key Points

Discussion

Implication

Cite This Study

Determinants of Thyroxine-Induced Cardiac Hypertrophy in Mice

Key Points

Discussion

Implication

Cite This Study

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