Triiodothyronine-enhanced left ventricular function after ischemic injury

Hypothyroidism is associated with profound left ventricular dysfunction. Brain-dead organ donors and patients undergoing cardiopulmonary bypass are chemically hypothyroid with significantly reduced circulating free triiodothyronine (T 3). To test the hypothesis that T 3 enhances left ventricular function in a hormonally deficient environment a total of 36 healthy New Zealand White rabbit hearts were studied using a modified Langendorff preparation with Krebs-Henseleit perfusate and intraventricular balloon. In 9 normal rabbit hearts a cumulative dose-response curve with logarithmically increasing doses of T 3 was obtained. The vehicle solution for T 3 dissolution served as control (n = 9). Left ventricular function was assessed from peak developed pressure at baseline and after T 3 administration. Triiodothyronine had no effect in normal hearts on peak developed pressure or end-diastolic pressure. In 18 rabbits, the acute effect of T 3 administration after ischemia was investigated. Preischemic left ventricular function was measured to serve as baseline, and hearts were subjected to 37 °C global ischemia. Triiodothyronine (n = 9) or vehicle (n = 9) was infused during reperfusion, and left ventricular peak developed pressure was measured at 30 and 60 minutes of reperfusion. Recovery of function (expressed as percent return of left ventricular peak developed pressure) was significantly improved within 15 minutes of reperfusion (65.0% ± 2.1% versus 80.2% ± 4.1%) and remained significantly improved throughout the reperfusion period ( p < 0.05 by analysis of variance). These data suggest that although T 3 possesses no inotropic properties, it significantly improves postischemic left ventricular function. The rapidity of the functional improvement suggests that these effects may be due to plasma membrane-mediated mechanisms.