ETA2023 Poster Presentations Thyroid Physiology in Periphery & Development Basic (9 abstracts)
Acute T3 administration reduces myocardial infarct size
Janina Pape 1 , Susanne Grund 2 , Kristina Piwellek 2 , Kristina Lorenz 3 , Friederike Langhauser 4 , Jens Mittag 5 , Lars Christian Möller 6 & Dagmar Führer 7
1University Hospital Essen; Department of Endocrinology, Essen, Germany; 2University Hospital Essen, Department of Endocrinology, Essen, Germany; 3Leibniz-Institut für Analytische Wissenschaften, Dortmund, Germany, Institute of Pharmacology and Toxicology, University of Wuerzburg, Würzburg, Germany; 4Universitätsklinikum Essen (Aör), Klinik für Neurologie, Essen, Germany; 5Universität Lübeck, Cbbm / Medi, Cbbm, Molecular Endocrinology, Universität zu Lübeck, Lübeck, Germany, Lübeck, Germany; 6University Hospital Essen, University Hospital Essen, Department of Endocrinology, Diabetes and Metabolism, Essen, Germany; 7Universitätsklinikum Essen, University Hospital Essen, Klinik für Endokrinologie und Stoffwechselerkrankungen, Essen, Germany
As thyroid hormones (TH) are essential for the normal heart function, a low TH state in ischemic cardiovascular events is often correlated to a poor prognosis. While clinical and experimental data suggests that TH intervention in acute myocardial infarction might be beneficial, a detailed insight in the mechanisms on TH action in IR injury or post infarct recovery of the heart is still lacking. In this study, we examined the effect of thyroid hormone pre- and postconditioning on infarct size and post-ischemic cardiac function in an isolated mouse heart ischemia/reperfusion setting and assessed classical cardioprotective pathways. We showed that T3 administration reduces infarct size in a dose dependent manner, but is equally effective when administered at baseline before ischemia or after ischemia at reperfusion. Additionally TH were beneficial for the recovery of left ventricular function after ischemia, with an increase in left ventricular developed pressure and a constant increase in coronary flow at reperfusion upon T3 administration. To contribute to the clarification of mechanisms underlying the cardioprotective effect of TH we also analyzed classical cardioprotective signaling pathways as well as eNOS phosphorylation at different time points at reperfusion. Here we could show that the enzyme activating phosphorylation of eNOS-Ser1177 did not differ upon T3 administration. However, increased phosphorylation of eNOS-Thr495, which is reducing NO production, could be observed. Co-administration of eNOS cofactor BH4 reversed the cardioprotective T3 effect, suggesting that T3 is reducing excessive NO levels in the myocardium.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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