Thyroid hormones improve cardiac function and decrease expression of pro-apoptotic proteins in the heart of rats 14 days after infarction

APOPTOSIS ◽  
2015 ◽  
Vol 21 (2) ◽  
pp. 184-194 ◽  
Author(s):  
Alexandre Luz de Castro ◽  
Rafael Oliveira Fernandes ◽  
Vanessa D. Ortiz ◽  
Cristina Campos ◽  
Jéssica H. P. Bonetto ◽  
...  
Keyword(s):  
Thyroid Hormones ◽  
Cardiac Function ◽  
Apoptotic Proteins

scholarly journals Thyroid Hormones within the Normal Range and Cardiac Function in the General Population: The EPIPorto Study

2020 ◽  
pp. 1-11
Author(s):  
João Sérgio Neves ◽  
Ricardo Fontes-Carvalho ◽  
Marta Borges-Canha ◽  
Ana Rita Leite ◽  
Sandra Martins ◽  
...  
Keyword(s):  
General Population ◽  
Thyroid Hormones ◽  
Cardiac Function ◽  
Normal Range

scholarly journals Thyroid Hormone Plays an Important Role in Cardiac Function: From Bench to Bedside

2021 ◽  
Vol 12 ◽  
Author(s):  
Hiroyuki Yamakawa ◽  
Tomoko S. Kato ◽  
Jaeduk Yoshimura Noh ◽  
Shinsuke Yuasa ◽  
Akio Kawamura ◽  
...  
Keyword(s):  
Thyroid Hormones ◽  
Cardiac Function ◽  
Cardiovascular System ◽  
Antiarrhythmic Agent ◽  
Current Knowledge ◽  
Cardiac Contractility ◽  
The Body ◽  
The Past ◽  
Systolic And Diastolic Function

Thyroid hormones (THs) are synthesized in the thyroid gland, and they circulate in the blood to regulate cells, tissues, and organs in the body. In particular, they exert several effects on the cardiovascular system. It is well known that THs raise the heart rate and cardiac contractility, improve the systolic and diastolic function of the heart, and decrease systemic vascular resistance. In the past 30 years, some researchers have studied the molecular pathways that mediate the role of TH in the cardiovascular system, to better understand its mechanisms of action. Two types of mechanisms, which are genomic and non-genomic pathways, underlie the effects of THs on cardiomyocytes. In this review, we summarize the current knowledge of the action of THs in the cardiac function, the clinical manifestation and parameters of their hemodynamics, and treatment principles for patients with hyperthyroid- or hypothyroid-associated heart disease. We also describe the cardiovascular drugs that induce thyroid dysfunction and explain the mechanism underlying the thyroid toxicity of amiodarone, which is considered the most effective antiarrhythmic agent. Finally, we discuss the recent reports on the involvement of thyroid hormones in the regulation of myocardial regeneration and metabolism in the adult heart.

Changes in Cardiac Function Following Administration of Thyroid Hormones in Thyroidectomised Rats

1985 ◽  
Vol 7 (2) ◽  
pp. 290-296 ◽  
Author(s):  
I. Brooks ◽  
S. B. Flynn ◽  
D. A. A. Owen ◽  
A. H. Underwood
Keyword(s):  
Thyroid Hormones ◽  
Cardiac Function

Carvedilol and thyroid hormones co-administration mitigates oxidative stress and improves cardiac function after acute myocardial infarction

2019 ◽  
Vol 854 ◽  
pp. 159-166 ◽  
Author(s):  
Vanessa Duarte Ortiz ◽  
Patrick Türck ◽  
Rayane Teixeira ◽  
Bruna Gazzi Lima-Seolin ◽  
Denise Lacerda ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Thyroid Hormones ◽  
Cardiac Function

Decreased myocardial function and myosin ATPase in hearts from diabetic rats

1983 ◽  
Vol 244 (4) ◽  
pp. H586-H591 ◽  
Author(s):  
D. W. Garber ◽  
J. R. Neely
Keyword(s):  
Heart Rate ◽  
Thyroid Hormones ◽  
Cardiac Function ◽  
Atpase Activity ◽  
Systolic Pressure ◽  
Serum Glucose ◽  
Left Ventricular ◽  
Myosin Atpase ◽  
Myosin Atpase Activity ◽  
Serum Thyroid Hormones

The effect of diabetes on cardiac function was determined in isolated rat hearts. Diabetes was induced by injection of alloxan (doses ranged from 37.5 to 60 mg/kg body wt), and the heart were removed and perfused in the working heart preparation. Doses of alloxan ranging from 37.5 to 42 mg/kg did not consistently alter cardiac function even though serum glucose was elevated and serum thyroid hormones were reduced. Injection of 45 mg/kg of alloxan caused a large increase in serum glucose and a larger decrease in thyroid hormones. In this case, ventricular function was more consistently depressed after 1-2 wk. Function was not altered 48 h after injection of 60 mg kg of alloxan. However, when animals were given 60 mg/kg of alloxan and then maintained on insulin for 7 days, depressed cardiac function developed within 4 days after the insulin treatment was stopped. The decline in function involved a decrease in heart rate peak systolic pressure, and left ventricular +dP/dt. It was associated with greatly reduced serum thyroid hormones (both T3 and T4) and lower ventricular Ca2+-activated myosin ATPase activity. Fasting of rats for 4 days also resulted in decreased serum T3 and T4, depressed cardiac function (although heart rate was unchanged), and lower Ca2+-activated myosin ATPase activity.

scholarly journals MON-587 Thyroid Hormones within the Normal Range and Cardiac Function in the General Population: The Epiporto Study

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
João Sérgio Neves ◽  
Marta Canha ◽  
Ricardo Fontes-Carvalho ◽  
Madalena von Haffe ◽  
Catarina Vale ◽  
...  
Keyword(s):  
General Population ◽  
Thyroid Hormones ◽  
Cardiac Function ◽  
Normal Range

scholarly journals Exogenous H2S regulates endoplasmic reticulum-mitochondria cross-talk to inhibit apoptotic pathways in STZ-induced type I diabetes

2017 ◽  
Vol 312 (3) ◽  
pp. E190-E203 ◽  
Author(s):  
Fan Yang ◽  
Xiangjing Yu ◽  
Ting Li ◽  
Jianjun Wu ◽  
Yajun Zhao ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Cardiac Function ◽  
Er Stress ◽  
Ultrastructural Changes ◽  
Type I ◽  
Cardiac Tissues ◽  
Mptp Opening ◽  
Cyt C ◽  
Apoptotic Proteins ◽  
Apoptotic Pathways

The upregulation of reactive oxygen species (ROS) is a primary cause of cardiomyocyte apoptosis in diabetes cardiomyopathy (DCM). Mitofusin-2 (Mfn-2) is a key protein that bridges the mitochondria and endoplasmic reticulum (ER). Hydrogen sulfide (H2S)-mediated cardioprotection is related to antioxidant effects. The present study demonstrated that H2S inhibited the interaction between the ER and mitochondrial apoptotic pathway. This study investigated cardiac function, ultrastructural changes in the ER and mitochondria, apoptotic rate using TUNEL, and the expression of ER stress-associated proteins and mitochondrial apoptotic proteins in cardiac tissues in STZ-induced type I diabetic rats treated with or without NaHS (donor of H2S). Mitochondria of cardiac tissues were isolated, and MPTP opening and cytochrome c (cyt C) and Mfn-2 expression were also detected. Our data showed that hyperglycemia decreased the cardiac function by ultrasound cardiogram, and the administration of exogenous H2S ameliorated these changes. We demonstrated that the expression of ER stress sensors and apoptotic rates were elevated in cardiac tissue of DCM and cultured H9C2 cells, but the expression of these proteins was reduced following exogenous H2S treatment. The expression of mitochondrial apoptotic proteins, cyt C, and mPTP opening was decreased following treatment with exogenous H2S. In our experiment, the expression and immunofluorescence of Mfn-2 were both decreased after transfection with Mfn-2-siRNA. Hyperglycemia stimulated ER interactions and mitochondrial apoptotic pathways, which were inhibited by exogenous H2S treatment through the regulation of Mfn-2 expression.

Thyroid Hormones and Cardiac Function

1989 ◽  
pp. 117-128
Author(s):  
Ofer Binah ◽  
Irit Rubinstein ◽  
Bella Felzen ◽  
Yechiel Sweed ◽  
Sela Mager
Keyword(s):  
Thyroid Hormones ◽  
Cardiac Function

scholarly journals Risk of neurally mediated syncope in hypothyroidism and obesity

2021 ◽  
Vol 129 (3) ◽  
Author(s):  
José Ramón Lanz-Luces ◽  
José Manuel Lanz-Luces ◽  
Luis Fernando Escobar Guzmán ◽  
José Daniel Lanz-Souquett ◽  
Héctor Aceituno ◽  
...  
Keyword(s):  
Weight Gain ◽  
Thyroid Hormones ◽  
Cardiac Function ◽  
Autonomic Dysfunction ◽  
Neurally Mediated Syncope

Introduction and rationale: Thyroid hormones participate in several known mechanisms of cardiac function, being compromised in hypothyroidism (HPT), when uncontrolled, is associated with weight gain. HPT and Obesity participate in autonomic dysfunction.

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