Facilitated recovery of cardiac performance by triiodothyronine following a transient ischemic insult.

Reperfusion following a transient ischemic insult has been shown to result in a delayed recovery of myocardial function. A reduction in plasma triiodothyronine (T3) has been reported in these acute cardiovascular challenges. To test whether the replacement of T3 can facilitate the recovery of myocardial function following a transient regional ischemia, we investigated cardiac performance for 3 h after a 15-min, left anterior descending coronary artery occlusion in a canine model. Three groups of dogs were studied: I--control (n = 10); II--receiving T3 (0.25 micrograms/kg i.v. and 0.25 micrograms/kg/h for 3 h, n = 9), and III--receiving T3 (0.25 micrograms/kg i.v. and 0.5 micrograms/kg/h for 3 h, n = 9). Three hours following reperfusion, the T3 level in blood was significantly decreased in group I. Concomitantly, local segmental shortening was reduced from preocclusion control levels in group I (15.2 to 5.1%, p < 0.05), but recovered in both treated groups. The endsystolic elastance (Ees) and the external work (EW) efficiency (EW/PVA) in group I were depressed from preocclusion control (Ees = 95.5 +/- 0.8%; EW/PVA = 90.2 +/- 1.8%, both p < 0.05), the effective arterial elastance (Ea) and ventriculoarterial coupling (Ea/Ees) in group I were still elevated from preocclusion control (Ea = 122.5 +/- 5.1%; Ea/Ees = 128.3 +/- 5.3%, both p < 0.05). But these measures of global cardiac performance in the treated groups recovered following reperfusion, and the extent of recovery was dose dependent. These data suggest that T3 facilitates recovery of the stunned myocardium by improvement in local and global contractile function, in ventriculoarterial coupling, and in the energy efficiency.