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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Growth and stress seem to share common intracellular pathways and activation of growth signaling can increase resistance to stress. Thyroid hormone induces cardiac hypertrophy and preconditions the myocardium against ischemia reperfusion injury. The present study investigated whether this response is mediated by renin-angiotensin system (RAS). RAS is shown to be activated in hyperthyroidism and is involved in the development of cardiac hypertrophy. Male Wistar rats were treated with L-thyroxin (25 microg/100 g, sc, od) for fourteen days, while normal rats served as controls. In addition, irbesartan (150 mg/kg po), a potent blocker of angiotensin II type 1 receptor (AT1), was given with L-thyroxin for fourteen days. Isolated hearts were perfused in Langendorff mode; after stabilization, they were subjected to 20 min zero-flow global ischemia and 45 min of reperfusion. Thyroxin induced cardiac hypertrophy, which was diminished with irbesartan administration. Post-ischemic recovery of function was increased in thyroxin-treated hearts as compared to controls while ischemic contracture was accelerated and intensified. Irbesartan did not abolish this response. In conclusion, blockade of angiotensin II type 1 receptor with irbesartan preserves thyroxin-induced cardioprotection while diminishing cardiac hypertrophy. It is likely that thyroxin-induced cardioprotection is due to a direct effect of thyroid hormone.
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PMID:Blockade of angiotensin II type 1 receptor diminishes cardiac hypertrophy, but does not abolish thyroxin-induced preconditioning. 1613 63

In the presence of angina pectoris in a premenopausal woman without significant risk factors for coronary disease, we have to rule out other causes of coronary lesion of non atherosclerotic origin. The relations between hyperthyroidism and the cardiovascular system are well known, but hyperthyroidism is responsable for less than 5% of all causes of chest pain. We present a clinical case of a 47 year old woman with typical chest pain and eletrocardiogram (EKG) suggesting coronary ischemia but with normal laboratory data. Anamnesis, clinical and the laboratory data confirmed the diagnosis of hyperthyroidism. Further investigation showed a normal coronary angiography. After treatment with radioiodine and the establishment of euthyroidism, the patient remained asymptomatic and EKG and myocardial scintilography were negative for ischemia. These results suggest a cause and effect relationship between thyroid overactivity and myocardial ischemia, implying a probable etiological role for hyperthyroidism in the clinical and EKG findings.
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PMID:Angina pectoris in patient with hyperthyroidism and normal angiography coronary. 1739 88

Autofluorescence response to oxygen supply modulation has been investigated in livers of rats under the hypermetabolic state associated to a pathological condition-hyperthyroidism-that is known to enhance hepatocyte metabolic activities involving both NAD, i.e. oxidative pathways engaged in ATP synthesis, and NADP, i.e. reductive bio-synthesis and antioxidant functions. Experiments have been performed on rats in normal condition or submitted to long-term thyroxine (T(4)) administration. Histological inspection did not show any appreciable morphological alteration in liver parenchyma; biochemical analysis indicated an increase in both NADP(+) and NADPH contents. Autofluorescence properties have been monitored in vivo, via a fiber optic probe, on exposed livers both during induction of global ischemia and after restoration of blood circulation. Alteration of oxygen supply modulated liver autofluorescence properties, mainly as to NAD(P)H contribution, in dependence of changes in pyridine coenzymes redox state. With respect to euthyroid, hyperthyroid rat livers exhibited higher autofluorescence signals in all phases of the experiment, and a faster signal decay time upon reoxygenation. The results have been interpreted on the basis of a larger content of NADPH-the coenzyme not directly oxidized in respiratory processes and likely providing an almost constant autofluorescence background contribution-and of uncoupling effects facilitating the respiratory NADH oxidation, associated with the hyperthyroid condition. The results obtained in the liver hypermetabolic model provide interesting perspectives for a further improvement of the diagnostic implications of autofluorescence.
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PMID:Autofluorescence properties of rat liver under hypermetabolic conditions. 1797 53

The cross-sectional epidemiological studies investigating hyperthyroidism as a risk factor for hypertension and stroke are not conclusive. Several case studies, however, indicate that persistent thyrotoxicosis aggravates neurological damage subsequent to a stroke. To test the hypothesis, we measured physiological and biochemical parameters in a model of transient focal ischemia in rats with prior induction of thyrotoxicosis to investigate its effects. Age- and weight-matched rats were made hyperthyroid prior to middle cerebral artery (MCA) occlusion and killed after 3 days of reperfusion. We then estimated neurological deficit scores, body temperature, circulating total and free thyroxine (fT(4)) levels, lipid peroxide and thiol levels, and lactate dehydrogenase activity. While the standard 2-h occlusion of MCA resulted in very high mortality in hyperthyroid animals, the 30-min MCA occlusion resulted in a significant increase in neurological deficits compared with sham-operated animals. We observed a twofold or more increase in circulating fT(4) levels in rats receiving thyroxine. The increase in infarct size directly correlated with the increased dose of thyroxine. A significant thyroxine dose-dependent increase in lipid peroxide (malondialdehyde levels, P<0.05), lactate dehydrogenase activity (P<0.01), and a significant decrease in protective thiol levels (P<0.05) were observed. The data support our hypothesis that thyrotoxicosis is an independent risk factor which contributes to the aggravation of post-stroke injury and death. The study results indicate a need to control thyrotoxicosis in elderly populations to reduce the risk.
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PMID:Pathophysiological basis for thyrotoxicosis as an aggravating factor in post-ischemic brain injury in rats. 1825 57

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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PMID:In hyperthyroid rats octylguanidine protects the heart from reperfusion damage. 1916 49

Atrial fibrillation (AF) is a complex condition with several possible contributing factors. The rapid and irregular heartbeat produced by AF increases the risk of blood clot formation inside the heart. These clots may eventually become dislodged, causing embolism, stroke and other disorders. AF occurs in up to 15% of patients with hyperthyroidism compared to 4% of people in the general population and is more common in men and in patients with triiodothyronine (T3) toxicosis. The incidence of AF increases with advancing age. Also, subclinical hyperthyroidism is a risk factor associated with a 3-fold increase in development of AF. Thyrotoxicosis exerts marked influences on electrical impulse generation (chronotropic effect) and conduction (dromotropic effect). Several potential mechanisms could be invoked for the effect of thyroid hormones on AF risk, including elevation of left atrial pressure secondary to increased left ventricular mass and impaired ventricular relaxation, ischemia resulting from increased resting heart rate, and increased atrial eopic activity. Reentry has been postulated as one of the main mechanisms leading to AF. AF is more likely if effective refractory periods are short and conduction is slow. Hyperthyroidism is associated with shortening of action potential duration which may also contribute to AF.
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PMID:The mechanisms of atrial fibrillation in hyperthyroidism. 1934 75

Hyperthyroidism elevates cardiovascular mortality by several mechanisms, including increased risk of ischemic heart disease. Therefore, therapeutic strategies, which enhance tolerance of heart to ischemia-reperfusion injury, may be particularly useful for hyperthyroid patients. One promising cardioprotective approach is use of agents that cause (directly or indirectly) A1 adenosine receptor (A1 receptor) activation, since A1 adenosinergic pathways initiate protective mechanisms such as ischemic preconditioning. However, previously we found great A1 receptor reserve for the direct negative inotropic effect of adenosine in isolated guinea pig atria. This phenomenon suggests that weakening of atria is a possible side effect of A1 adenosinergic stimulant agents. Thus, the goal of the present investigation was to explore this receptor reserve in hyperthyroidism. Our recently developed method was used that prevents the rapid intracellular elimination of adenosine, allowing sufficient time for exogenous adenosine administered for the generation of concentration-response curves to exert its effect. Our method also allowed correction for the bias caused by the consequent endogenous adenosine accumulation. Our results demonstrate that thyroxine treatment does not substantially affect the A1 receptor reserve for the direct negative inotropic effect of adenosine. Consequently, if an agent causing A1 receptor activation is administered for any indication, the most probable adverse effect affecting the heart may be a decrease of atrial contractility in both eu- and hyperthyroid conditions.
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PMID:Approximation of A1 adenosine receptor reserve appertaining to the direct negative inotropic effect of adenosine in hyperthyroid guinea pig left atria. 2417 21

Hyperthyroidism, known to have deleterious effects on heart function, and is associated with an enhanced metabolic state, implying an increased production of reactive oxygen species. Tamoxifen is a selective antagonist of estrogen receptors. These receptors make the hyperthyroid heart more susceptible to ischemia/reperfusion. Tamoxifen is also well-known as an antioxidant. The aim of the present study was to explore the possible protective effect of tamoxifen on heart function in hyperthyroid rats. Rats were injected daily with 3,5,3'-triiodothyronine at 2mg/kg body weight during 5 days to induce hyperthyroidism. One group was treated with 10mg/kg tamoxifen and another was not. The protective effect of the drug on heart rhythm was analyzed after 5 min of coronary occlusion followed by 5 min reperfusion. In hyperthyroid rats not treated with tamoxifen, ECG tracings showed post-reperfusion arrhythmias, and heart mitochondria isolated from the ventricular free wall lost the ability to accumulate and retain matrix Ca(2+) and to form a high electric gradient. Both of these adverse effects were avoided with tamoxifen treatment. Hyperthyroidism-induced oxidative stress caused inhibition of cis-aconitase and disruption of mitochondrial DNA, effects which were also avoided by tamoxifen treatment. The current results support the idea that tamoxifen inhibits the hypersensitivity of hyperthyroid rat myocardium to reperfusion damage, probably because its antioxidant activity inhibits the mitochondrial permeability transition.
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PMID:Antiarrhythmic effect of tamoxifen on the vulnerability induced by hyperthyroidism to heart ischemia/reperfusion damage. 2492 30

Oxidative stress results from either overproduction of free radicals or insufficiency of several anti-oxidant defense systems. It leads to oxidation of main cellular macromolecules and a resultant molecular dysfunction. Thyroid hormones regulate oxidative metabolism and, thus, play a role in free radical production. Studies evaluating oxidative stress in patients with hypothyroidism and hyperthyroidism have been encountered in recent years; however, oxidative status in patients with euthyroid autoimmune thyroiditis (AIT) was not investigated previously. Thirty-five subjects with euthyroid AIT and 35 healthy controls were enrolled in the study. Serum oxidative status was determined by the measurement of total anti-oxidant status (TAS), total oxidant status (TOS), ischemia-modified albumin (IMA), and oxidized-low density lipoprotein (ox-LDL) levels. Serum TAS levels were significantly lower (p<0.001), while serum TOS levels and IMA levels were significantly higher (p<0.001 and p=0.020, respectively) in patients compared to controls. In both groups, ox-LDL levels were similar (p=0.608). Serum TAS levels were negatively correlated with anti-thyroid peroxidase and anti-thyroglobulin (anti-TG) levels (rho=-0.415, p=0.001 and rho=-0.484, p<0.001, respectively). Serum TOS was positively correlated with anti-TG levels (rho=0.547, p<0.001). Further, TAS was positively correlated with free T4 levels (r=0.279, p=0.043). No correlation was observed between thyrotropin, free T3 levels, and TOS and TAS levels. These results suggest that oxidants are increased, and anti-oxidants are decreased in patients with euthyroid AIT, and oxidative/anti-oxidative balance is shifted to the oxidative side. Increased oxidative stress might have a role in thyroid autoimmunity.
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PMID:Assesment of oxidative status and its association with thyroid autoantibodies in patients with euthyroid autoimmune thyroiditis. 2515 37

Hyperthyroidism represents an increased risk factor for cardiovascular morbidity, especially when the heart is subjected to an ischemia/reperfusion process. The aim of this study was to explore the possible protective effect of the nucleotide citicoline on the susceptibility of hyperthyroid rat hearts to undergo reperfusion-induced damage, which is associated with mitochondrial dysfunction. Hence, we analyzed the protective effect of citicoline on the electrical behavior and on the mitochondrial function in rat hearts. Hyperthyroidism was established after a daily i.p. injection of triiodothyronine (at 2 mg/kg of body weight) during 5 days. Thereafter, citicoline was administered i.p. (at 125 mg/kg of body weight) for 5 days. In hyperthyroid rat hearts, citicoline protected against reperfusion-induced ventricular arrhythmias. Moreover, citicoline maintained the accumulation of mitochondrial Ca(2+), allowing mitochondria to reach a high transmembrane electric gradient that protected against the release of cytochrome c. It also preserved the activity of the enzyme aconitase that inhibited the release of cytokines. The protection also included the inhibition of oxidative stress-induced mDNA disruption. We conclude that citicoline protects against the reperfusion damage that is found in the hyperthyroid myocardium. This effect might be due to its inhibitory action on the permeability transition in mitochondria.
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PMID:Cardioprotective properties of citicoline against hyperthyroidism-induced reperfusion damage in rat hearts. 2558 88


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