Thorac Cardiovasc Surg 2000; 48(1): 27-33
DOI: 10.1055/s-2000-8892
Original Cardiovascular
© Georg Thieme Verlag Stuttgart · New York

Acute Triiodothyronine Administration Does Not Reverse Depressed Contractile Performance Following Catecholamine Exposure in Isolated Rat Cardiomyocytes[1]

M. F. Castell, M. Doll, N. Stumpf, C.-F. Vahl, S. Hagl
  • Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany
Further Information

Publication History

Publication Date:
31 December 2000 (online)

Background: It has been previously suggested that triiodothyronine (T3) may reverse depressed cardiac contractile performance occurring affer excessive catecholamine stimulation. We therefore investigated the effects of T3 on intracellular calcium transients and contractile performance in isolated ventricular rat myocytes. Methods: Isolated rat myocytes were loaded with the calcium indicator FURA-2/AM (50 µmol/L) and superfused with Krebs-Henseleit solution (pH 7.4). Cells were illuminated by ultraviolet light and fluorescent images obtained with a target camera at 340 nm and 380 nm excitation wavelengths (ratio method). Simultaneous measurements of calcium transients and cell shortening (35° C, electrical field stimulation: 0.5 Hz) were done. At steady state conditions, FURA-2 loaded myocytes were superfused for 60 min with epinephrine (0.1 µmol/L). After 60 min the effect of T3 (10 µmol/L) on calcium transients and shortening were measured. As control, only the effect of 10 µmol/L T3 was analyzed. Results: Epinephrine significantly increased cell shortening and FURA-2 signals to 148.6 ± 8.8 % and 109.5 ± 3.1 % (p < 0.01: n = 21; 5 min) respectively. With longer epinephrine exposure, the increase in cell shortening continuously declined to 134.6 ± 7.9 % with no change in FURA-2 fluorescence. Acute administration of T3 after epinephrine exposure lowered contractile performance from 136.2 ± 15.5 % to 102 ± 8.2 %, after 10 minutes. In control experiments acute administration of T3 increased basal contractile response from 100 % to 115.8 ± 3.3 % (p < 0.01; n = 8; 5 min). Conclusions: This study confirms previous reports of impaired cardiac function after high catecholamine exposure. High catecholamine exposure is associated with a desensitization of contractile proteins for calcium. Acute T3 administration increased contractility in untreated myocytes, but further depressed myocyte shortening in epinephrine-treated cells. Our results show that T3 is ineffective at restoring myocardial contractility after excessive catecholamine stimulation.

1 Presented in part at the Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery, Dresden, February 1999

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1 Presented in part at the Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery, Dresden, February 1999

Dr. M. F. Castell

Chirurgische Klinik Abteilung Herzchirurgie

Im Neuenheimer Feld 110

D-69120 Heidelberg

Germany

Email: Maria_Fernanda.Cas@urz.uni-heidelberg.de

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