Effects of triiodothyronine on stunned myocardium

Administration of thyroid hormone, triiodothyronine (T3), causes numerous cardiovascular effects such as increases in stroke volume, cardiac output, heart rate, and myocardial contractility, and decreases in systemic vascular resistance. Along with other stressors, cardiopulmonary bypass (CPB) has been associated with reduced levels of T3. We examined the effects of T3 on early postischemic myocardial recovery in rabbit hearts subjected to crystalloid perfusion to simulate a low T3 state, and in pig hearts following global ischemia due to CPB. Studies using the former system showed that T3 administration results in significantly improved developed pressure after reperfusion of mildly ischemic hearts compared to controls, without producing inotropic effects. In more severely stunned rabbit hearts, physiologic and 10 times physiologic doses of T3 produced significantly improved (p < 0.05) stroke work end-diastolic length compared to placebo treatment. T3 treated pigs undergoing CPB and subjected to 30 minutes of global normothermic ischemia experienced significantly enhanced recovery of left ventricular contractility compared to controls at 90 and 120 minutes post reperfusion. Neither placebo nor T3 affected myocardial adenosine triphosphate levels. These data show that T3 enhances recovery from myocardial stunning without producing acute inotropic effects.