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

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