Acute Increase in Cardiac Performance After Triiodothyronine: Blunted Response in Amiodarone-Treated Pigs

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SummaryChronic hyperthyroidism is associated with increased myocardial contractility. The direct cardiac effect occurs through triiodothyronine (T3)-mediated synthesis of specific proteins. More recent studies have suggested that T3 may increase cardiac performance acutely, independent of protein neosynthesis. We wished to evaluate whether acutely administered T3 exerts an acute, dose-dependent hemodynamic response and adverse effects in normal and amiodarone-treated pigs. Closed-chest, fully anesthetized animals were used. For the dose-response study, 4 control pigs received increasing doses (4, 20, 200, and 2,000 μ, g) T3 at 15-min intervals, and the hemodynamic response and ECG features were monitored continuously. Another 4 control pigs received a single bolus of either of the four doses and were monitored for 60 min. Eight pigs that had received amio-darone (800 mg/day) for 10 days and 8 pigs that served as untreated controls were used in the hemodynamic study. Hemodynamic parameters were evaluated before and after a single bolus injection of 20 μ,g T3. Observation lasted no longer than 45 min to assure that synthesis of new proteins would not contribute to changes in cardiac ability. T3 gave rise to a dose-dependent increase in cardiac performance within a certain dose range. Arrhythmias were also dose dependent and were not observed for the two lower doses. By 15 min after administration of 20 μ.g T3, cardiac contractility had increased significantly and continued to increase throughout the observation period. After 45 min, peak left ventricular pressure (LVP) was increased by a mean of 27% (p < 0.001) and 19% (p = 0.013) in controls and amiodarone-treated pigs. Mean arterial pressure (MAP) was increased by 33% (p = 0.002) and 19% (NS). Cardiac output was increased by a mean of 47% (p = 0.04) and 27% (p = 0.003), and LV contractile force (+ dP/dt) was increased by 90% (p = 0.04) and 63% (p < 0.02). The response was significantly less for amiodarone-treated pigs than for controls (p < 0.03). Pre- and afterload remained constant in all animals. T3 exerts an acute, positive, and dose-related effect on cardiac contractility in pigs without cardiac disease. The mechanism is hypothesized to be caused by altered permeability of the cardiac sarcolemma to Ca2+. Amiodarone's Ca2+ channel blocking properties may have contributed to the blunted hemodynamic response observed in animals pre-treated with the drug

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