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Ann Thorac Surg 1994;58:851-856
© 1994 The Society of Thoracic Surgeons

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Articles

Direct effects of acute administration of 3, 5, 3' triiodo-L-thyronine on myocyte function

Divisions of Cardiothoracic Surgery and Adult Cardiology, Medical University of South Carolina, Charleston, South Carolina USA

Accepted for publication February 8, 1994.

^_* Address reprint requests to Dr Walker, Division of Cardiothoracic Surgery, Medical University of South Carolina, 171 Ashley Ave, Charleston, SC 29425.

Recent studies have suggested that acute administration of 3, 5, 3' triiodo-L-thyroninc (T₃) may increase ventricular performance; however, the direct cellular effects of acute T₃ administration are not understood. The objectives of this study were to determine (1) whether T₃ acts directly on the cardiac muscle cell (myocyte) itself, and (2) whether T₃ acts independently of the myocyte β-adrenergic receptor. Accordingly, isolated myocyte function was examined using video-microscopy in normal porcine myocytes (n = 60) in the control state and in the presence of increasing T₃ concentrations (10 to 500 pmol/L). T₃ caused myocyte shortening extent, shortening velocity, and lengthening velocity to increase in a dose-dependent manner. For example, shortening velocity increased from 49.2 ± 4.3 µm/s at baseline to 66.5 ± 6.1 µm/s with 100 pmol/L T₃ (p < 0.05). β-Adrenergic stimulation with 25 nmol/L isoproterenol increased shortening velocity to 97.6 ± 5.7 µm/s; isoproterenol with T₃ increased shortening velocity further to 168.5 ± 10.9 µm/s. Analysis of variance revealed that this increase with T₃ was independent of and additive to the β-adrenergic receptor system. In summary, T₃ caused a dose-dependent increase in myocyte contractile performance, and these effects were independent of and additive to β-adrenergic receptor stimulation. Thus, acute T₃ administration may provide a novel modality to improve left ventricular contractile function independent of the β-adrenergic receptor system.

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