Hypothyroidism provides resistance to reperfusion injury following myocardium ischemia

Bobadilla, Israel; Franco, Martha; Cruz, David; Zamora, José; Robles, Sandra G.; Chávez, Edmundo

doi:10.1016/s1357-2725(01)00016-4

Cited by 15 publications

(17 citation statements)

References 30 publications

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“…In recent years, our laboratory has been addressing the subject of the role of thyroid hormone as a regulator of reperfusion damage and mitochondrial permeability transition. Our findings revealed that hypothyroidism protects from pore opening (Chávez et al, 1998) and heart reperfusion damage (Bobadilla et al, 2001). In a similar context, Tenorio-Velázquez et al (2005) have demonstrated that hypothyroidism attenuates oxidative stress and renal injury induced by ischemia/ reperfusion.…”

Section: Introductionsupporting

confidence: 65%

Hypothyroidism provides resistance to kidney mitochondria against the injury induced by renal ischemia-reperfusion

Zazueta¹,

Franco²,

Correa³

et al. 2007

Life Sciences

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Section: Introductionsupporting

confidence: 65%

Hypothyroidism provides resistance to kidney mitochondria against the injury induced by renal ischemia-reperfusion

Zazueta¹,

Franco²,

Correa³

et al. 2007

Life Sciences

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“…Recently, we found that hypothyroidism renders liver mitochondria resistant to undergo permeability transition [14]. In agreement, we further demonstrated that hypothyroidism provides resistance to the myocardium against reperfusion injury [15]. To explain these findings we proposed that the lack of cardiolipin in the lipid phase of the inner mitochondrial membrane restrains the shift of adenine nucleotide translocase (ANT) to the nonspecific transmembrane pore.…”

Section: Introductionmentioning

confidence: 61%

“…The ischemic period lasted 5 min. This time was selected in agreement with previous reports [15,27,38]. Nevertheless, to get a better insight about the myocardial damage, experiments with 20 min of reperfusion were also performed.…”

Section: Heart Reperfusionmentioning

confidence: 99%

In hyperthyroid rats octylguanidine protects the heart from reperfusion damage

Pavón

Aranda

Garcı́a

et al. 2009

Endocr

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Hyperthyroidism sensitizes the heart for reperfusion injury. As known, mitochondrial permeability transition underlies reperfusion heart damage. This study was undertaken to explore the protective effect of octylguanidine (OG), an inhibitor of permeability transition, on hearts from hyperthyroid rats subjected to ischemia/reperfusion. Hyperthyroidism was induced by a daily injection of 2 mg T3/kg body weight for 5 days. OG was injected at a dose of 5 mg/kg body weight. It was found that the amine protects against reperfusion-induced permeability transition, i.e., mitochondria from hyperthyroid rats, treated with OG, retained accumulated Ca(2+), similarly to control mitochondria. OG maintained post reperfusion cardiac frequency in hyperthyroid rats at 429 +/- 16 in comparison to control and T3 treated rats (70 +/- 12 and 71 +/- 2, respectively). We also found that OG diminished the post reperfusion accumulation of IFNgamma from 34.3 +/- 2.5 to 18.7 +/- 1.35, IL-6 from 38.5 +/- 4.5 to 15.1 +/- 0.12, IL-1 from 16.78 +/- 0.73 to 12.19 +/- 1.54, and TNFalpha from 45.05 +/- 3.14 to 29.85 +/- 4.3 (pg/50 microg myocardial tissue). It is concluded that OG inhibits the hypersensitivity of the hyperthyroid myocardium to undergo reperfusion damage due to its inhibitory action on the permeability transition pore.

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“…This might be true in hypothyroid condition, but potentially harmful if the heart has been exposed to excess thyroid hormone. Bobadilla and his associates reported that hypothyroidism provides enzymatic and histological resistance to reperfusion injury following myocardial ischemia [20]. Oxidative damage on lipids, glutathione, and DNA caused by thyroid hormone was also reported in the mouse heart [21].…”

Section: Discussionmentioning

confidence: 97%

“…However, it is reported that lipid peroxidation is augmented through the increased oxidative stress in hyperthyroidism [8]. And hypothyroidism provides resistance to reperfusion injury following myocardial ischemia [9]. It remains controversial if the additional thyroid hormone treatment contributes to better myocardial function in euthyroid patients.…”

Section: Introductionmentioning

confidence: 99%

Hyperthyroidism Causes Mechanical Insufficiency of Myocardium with Possibly Increased SR Ca<sup>2+</sup>-ATPase Activity

et al. 2003

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Hyperthyroidism is accompanied by important changes in hemodynamics and cardiac functions. These include clinical manifestation such as an increased cardiac contractility and heart rate, as well as decreased peripheral vascular resistance. Increased nitric oxide production [1,2], which may affect the peripheral vascular resistance, and shorter time-to-peak of twitch tension, which may be associated with an increased cardiac contractility, have been reported in the hyperthyroid state [3]. Thyroid hormone is also known to affect the gene expression; major components of myocardial contraction, including sarcoplasmic reticulum (SR) Ca 2ϩ -ATPase (SERCA2) [4]; myosin heavy chains (MHC) [5]; and other protein expressions, such as glucose transporter GLUT4 facilitating glucose uptake [6]. Glucose metabolism is very important to providing energy not only for myocardial contraction, but also for the maintenance of intracellular ionic balances.Thyroid hormone is a potential contributor to a bet- Japanese Journal of Physiology, 53, 411-416, 2003 Key words: hyperthyroidism, myocardial metabolism, SR Ca 2ϩ ATPase, excitation-contraction coupling. Abstract:Hyperthyroidism is known to affect multiple organ functions, and thyroid hormone has been known to improve myocardial function in a failing heart. The purpose of this study is to elucidate the functional and metabolic effects of thyroid hormone on myocardium in a rat model exposed to long-term excess thyroid hormone, particularly focusing on the SR Ca 2ϩ -ATPase (SERCA2) function. 3,5,3Ј-Triiodo-L-thyronine (T3), or the vehicle, was subcutaneously given for 4 weeks (T3 and control [C] group). Bolus I.V. Thapsigargin (TG) was used to test the SERCA2 function (C-TG and T3-TG) in Langendorff perfused heart. Myocardial functions such as LVdeveloped pressure (LVDP; mmHg), ϮdP/dt (mmHg/s), (ms), and oxygen consumption (MVO 2 ; ml/min/g wt) were measured. SERCA2 and GLUT4 protein level were also evaluated by Western immunoblotting. Left ventricle to body weight (LV/BW) ratio was significantly higher in the T3 group. Both negative dP/dt and were significantly decreased by TG. It is interesting that the decrement of negative dP/dt and attained by TG was significantly larger in the hyperthyroid group (T3-TG) than in a normal heart (C-TG). SERCA2 and GLUT4 protein levels were not significantly different between control and the T3 group. We conclude that prolonged exposure to thyroid hormone causes hypertrophy of the myocardium and an augmentation of the SR Ca 2ϩ ATPase activity. Care must be taken in hyperthyroid heart during the ischemia-reperfusion process where the SRECA2 function is inhibited.

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Hypothyroidism provides resistance to reperfusion injury following myocardium ischemia

Cited by 15 publications

References 30 publications

Hypothyroidism provides resistance to kidney mitochondria against the injury induced by renal ischemia-reperfusion

Hypothyroidism provides resistance to kidney mitochondria against the injury induced by renal ischemia-reperfusion

In hyperthyroid rats octylguanidine protects the heart from reperfusion damage

Hyperthyroidism Causes Mechanical Insufficiency of Myocardium with Possibly Increased SR Ca<sup>2+</sup>-ATPase Activity

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