Triiodothyronine improves contractile recovery of human atrial trabeculae after hypoxia/reoxygenation.

BACKGROUND

In patients undergoing interventional or surgical coronary revascularization, subclinical hypothyroidism is common and associated with worse outcome, including the need for postoperative inotropic support. In isolated rat hearts with global ischemia/reperfusion, exogenous triiodothyronine (T3) reduces infarct size. Aim of this study was, to investigate whether or not exogenous T3 protects human myocardium from ischemia/reperfusion injury.

METHODS

Right atrial trabeculae from patients undergoing routine coronary artery bypass grafting were isolated and transferred to Tyrode's buffer. Electrically initiated (1 Hz) contractile stress (mN/mm) was recorded for 10 min at baseline (95% O/ 5% CO, glucose). Sixty min hypoxia were induced by changing buffer gas and increasing stimulation rate (95% N/ 5% CO, choline chloride, 3 Hz) before return to reoxygenation for 30 min. T3 (500 μg/l) vs. NaOH (solvent control) was administered A) throughout (n = 11 vs. n = 9) or B) only 15 min before and during reoxygenation (n = 12 vs. n = 13). Western blot analyses of established cardioprotective signaling proteins were performed.

RESULTS

At baseline, contractile stress was comparable. T3 improved the cumulative recovery of contractile stress during reoxygenation from 41 ± 16 with NaOH to 55 ± 11% of baseline with T3, when given continuously in A or from 52 ± 13 with NaOH to 63 ± 11% of baseline with T3 when given just before and during reoxygenation in B. The ratio of mitochondrial complex I matrix arm to membrane NADH:ubiquinone oxidoreductase subunits (NDUF)V2 to NDUFA9 was reduced, reflecting increased complex I activity.

CONCLUSION

T3 increases contractile recovery of human right atrial trabeculae from hypoxia/reoxygenation.