Effect of triiodothyronine administration in experimental myocardial injury.

Twelve healthy pigs were subjected to a 20-min, period of regional myocardial ischemia by snaring the left anterior descending coronary artery (LAD) between its first and second diagonal branches. The resulting myocardial injury caused significant acute hemodynamic impairments. Cardiac index declined significantly during reperfusion interval and returned to preischemic level by postoperative day 7. Plasma total triiodothyronine (TT3), free triiodothyronine (FT3) and free fatty acid (FFA) decreased gradually and reached the nadir at 6 h after LAD occlusion. In contrast, plasma reverse triiodothyronine (rT3) increased progressively after LAD occlusion and reperfusion. To investigate the effect of T3 on ischemic myocardium, T3 (0.2 microgram/kg/dose; n = 5) or saline (placebo; n = 6) was administered immediately, 30 min, 60 min, 90 min, and 120 min after reperfusion. Plasma TT3 and FT3 increased dramatically after triiodothyronine supplement but declined to presichemic level at six h after LAD occlusion. The pigs treated with T3 demonstrated a rapid improvement in cardiac index over the reperfusion interval, whereas cardiac index in the placebo group remained depressed. Myocardial oxygen consumption estimated by rate pressure product showed no difference between placebo and T3-treated groups. Oxygen extraction as O2 saturation difference between aorta and coronary sinus was less in T3-treated group. Nine pigs (four in the T3-treated group and five in the placebo group) were subjected to euthanasia with hypertonic KCl solution on postoperative day 7. Myocardial infarct size determined by triphenyltetrazolium chloride (TTC) tissue enzyme staining technique was not significantly different between T3-treated and placebo groups. We concluded that this animal model is a useful model of myocardial injury simulating "euthyroid sick syndrome" as seen in patients with cardiopulmonary bypass, and T3 supplementation after reperfusion significantly enhanced postischemic left ventricular functional recovery but did not affect myocardial oxygen consumption and myocardial infarct size.