UMLS:C0151744 - FACTA Search

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Query: UMLS:C0151744 (myocardial ischemia)
31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cigarette smoking has been implicated in the pathogenesis of ischemic heart disease, emphysema, obstructive lung disease and neoplastic disorders. More than 1000 constituents of smoke, including many oxidants, pro-oxidants, free radicals and reducing agents, have been identified. The activities of erythrocyte superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), which are the important components of antioxidant defense system, were measured in 100 healthy volunteers. This study included heavy smokers (consuming cigarettes > or = 20 per day; n=30, group I), light smokers (consuming cigarettes<20 per day; n=30, group II), passive smokers (exposed to cigarette smoke in the indoor environment; n=20, group III), and non-smokers (n=20, the control group). While activities of SOD and CAT in erythro cytes were significantly lower in groups I, II and III than in the control group (p<0.01 for all), mean erythrocyte GSH-Px activity in group III was higher than that in groups l, II and in controls. These results suggest that the increased oxidative stress occurs in smokers, owing to the free radicals present in smoke. It might cause a decrease in antioxidant enzyme activities and oxidant/antioxidant imbalance. We also observed that passive smokers were affected by the environmental smoke to the same extent as active smokers.
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PMID:The changes of superoxide dismutase, catalase and glutathione peroxidase activities in erythrocytes of active and passive smokers. 1221 58

Limited information is available on the effects of chronic mercury exposure in relation to the risk of cardiovascular disease (CVD). It is known from in vitro and in vivo studies that Hg can promote lipid peroxidation through promotion of free radical generation, and interaction with antioxidative enzymes and reduction of bioavailable selenium. The objective of the study was to test the hypothesis that long-term past occupational exposure to elemental Hg (Hg0) can modify antioxidative capacity and promote lipid peroxidation in miners. The study population comprised 54 mercury miners and 58 workers as the control group. The miners were examined in the post-exposure period. We evaluated their previous exposure to Hg0, the putative appearance of certain nonspecific symptoms and signs of micromercurialism, as well as the main behavioural and biological risk factors for CVD, and determined: 1) Hg and Se levels in blood and urine, 2) antioxidative enzymes, Cu/Zn superoxide dismutase (CuZn-SOD), catalase (CAT), and selenoenzyme glutathione peroxidase (GSH-Px) activity in erythrocytes as indirect indices of free radical activity, 3) pineal hormone melatonin (MEL) in blood and urine, and 4) lipid hydroperoxides (LOOHs) and malondialdehyde (MDA) as lipid peroxidation products. The mercury miners were intermittently exposed to Hg0 for periods of 7 to 31 years. The total number of exposure periods varied from 13 to 119. The cumulative U-Hg peak level varied from 794-11,365 microg/L. The current blood and urine Hg concentrations were practically on the same level in miners and controls. Miners showed some neurotoxic and nephrotoxic sequels of micromercurialism. No significant differences in behavioural and biological risk factors for CVD were found between miners and controls. A weak correlation (r = 0.36, p < 0.01) between systolic blood pressure and average past exposure U-Hg level was found. The mean P-Se in miners (71.4 microg/L) was significantly lower (p < 0.05) than in the controls (77.3 microg/L), while the mean U-Se tended to be higher (p < 0.05) in miners (16.5 microg/g creatinine) than in the controls (14.0 microg/g creatinine). Among antioxidative enzyme activities, only CAT in erythrocytes was significantly higher (p < 0.01) in miners (3.14 MU/g Hb) than in the controls (2.65 MU/g Hb). The mean concentration of B-MEL in miners (44.3 ng/L) was significantly higher (p < 0.01) than in the controls (14.9 ng/L). The mean value of U-MEL sulphate (31.8 microg/L) in miners was significantly lower (p < 0.01) than in the control group (46.9 microg/L). Among the observed lipid peroxidative products, the mean concentration of U-MDA was statistically higher (p < 0.01) in miners (0.21 micromol/mmol creatinine) than in the controls (0.17 micromol/mmol creatinine). In the group of miners with high mercury accumulation and the presence of some nonspecific symptoms and signs of micromercurialism, the results of our study partly support the assumption that long-term occupational exposure to Hg0 enhances the formation of free radicals even several years after termination of occupational exposure. Therefore, long-term occupational exposure to Hg0 could be one of the risk factors for increased lipid peroxidation and increased mortality due to ischaemic heart disease (ICH) found among the mercury miners of the Idrija Mine.
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PMID:The impact of long-term past exposure to elemental mercury on antioxidative capacity and lipid peroxidation in mercury miners. 1513 89

Prospective epidemiological studies have shown that the incidence of numerous cardiovascular pathologies is correlated with body selenium status. However, it remains unclear whether selenium status also influences the outcome of myocardial infarction. The aim of the present study was to test whether dietary selenium intake affects myocardial necrosis induced by transient regional ischemia in vivo in rats. For this purpose, male Wistar rats received either a high-selenium (High-Se: 1.5 mg of Se/kg) or a low-selenium (Low-Se: 0.05 mg of Se/kg) diet for 10 weeks. Animals were subjected to 30 min of myocardial ischemia induced by coronary artery ligation followed by 60 min of reperfusion. Pre- and postischemic blood samples were collected for glutathione (GSH and GSSG) determination and for glutathione peroxidase (GSH-Px) assessment. Our results show that high-selenium intake reduces myocardial infarct size (High-Se: 25.16 +/- 1.19% versus Low-Se: 36.51 +/- 4.14%, p < 0.05), preserves postischemic GSH/GSSG ratio (High-Se: 1.37 +/- 0.37 versus Low-Se: 0.47 +/- 0.10, p < 0.05), increases plasma GSH-Px activity, and improves postischemic mean arterial pressure. In conclusion, preischemic body selenium status is a major determinant of the outcome of myocardial ischemia in vivo in rats probably because it influences the cellular redox status.
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PMID:Preischemic selenium status as a major determinant of myocardial infarct size in vivo in rats. 1524 60

Cardiac ischemia reperfusion leads to oxidative stress and poor physiological recovery. Selenium deficiency down-regulates thioredoxin reductase (Txnrd) and glutathione peroxidase (Gpx) activity, impairing recovery from ischemia-reperfusion. Furthermore, selenium supplementation has been shown to be cardioprotective and lessens oxidative stress in reperfused rat hearts. In this study we have investigated the role of selenium in the mRNA expression of these, and related antioxidant proteins, post ischemia-reperfusion. Male rats were fed varying doses of selenium for five weeks. Hearts were isolated and perfused using the Langendorff method with 22.5 min of global ischemia and 45 min reperfusion. RNA was extracted for quantitative real-time PCR analysis of glutathione peroxidase (Gpx)-1 and 4, glutathione reductase (Gsr), thioredoxin peroxidase-2 (Prdx2), thioredoxin (Txn) and thioredoxin reductase (Txnrd)-1 and 2 gene expression. Selenium deficiency produced significant reductions in Gpx-1, Gpx-4, Prdx2, Txnrd-1 and Txnrd-2 expression. Conversely, selenium supplementation of 1000 microg/kg significantly up-regulated Gpx-1, Gpx-4, Txn, Txnrd-1 and Txnrd-2 transcription. Our results show selenium modulates the cardiac mRNA expression of thioredoxin and glutathione related enzymes post ischemia-reperfusion, and impacts on tolerance to ischemia-reperfusion.
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PMID:Effects of dietary selenium on post-ischemic expression of antioxidant mRNA. 1579 62

Previous studies have demonstrated increased serum copper and iron levels and decreased selenium and zinc levels in patients with myocardial infarction. Furthermore, the prognostic value of the levels of trace elements in myocardial infarction has been stressed. We examined serum levels of Cu, Fe, Zn and Se, as well as glutathione peroxidase (GPx), a selenoenzyme with antioxidant properties, and C-reactive protein (CRP), a marker of inflammation, in acute coronary syndromes (ACS) regarding their relationship to cardiac troponins and creatine kinase-MB mass (CK-MBm), important prognostic markers. Serum trace elements, GPx activity and CRP were determined in 70 patients with ACS who were admitted within 12 h after the onset. Differences in these parameters were evaluated in three groups of patients divided according to the levels of cardiac markers: group III consisted of patients with high increases in cTnT, cTnI and CK-MBm (> or =0.9 ng/mL, > or =1.0 ng/mL, > or =30 ng/mL, respectively), patients with milder increases in these markers were included in groups II and I consisted of patients with values just above the upper reference limits. Serum Fe levels increased significantly in group II and even more prominently in group III compared to group I (p = 0.04, 0.002, respectively). There was no significant difference between groups II and III. The increase in serum Cu was significant in group III compared to both groups II and I (p = 0.04, 0.001, respectively). There was no significant difference between groups I and II regarding Cu and Zn. The decrease in serum Se and GPx levels was significant only between groups III and I (p = 0.004 for Se and p = 0.0001 for GPx). CRP levels showed a significant increase in group III compared to groups II and I (p = 0.03 and 0.001). CRP showed a significant positive and GPx a significant negative correlation to the cardiac markers cTnT, cTnI and CK-MBm. Cu was positively correlated to all cardiac markers, while the positive correlation between Fe and cardiac markers was significant only for cTnI. Both Zn and Se were negatively correlated to cTnT, and Se was also to cTnI. In conclusion, the increase in serum levels of Cu and Fe and the decrease in serum levels of Zn and Se in patients with higher levels of troponins and CK-MBm imply that trace element levels are related to the degree of myocardial damage and thus may play a role in the pathogenesis of ischemic heart disease. The strong correlations between cardiac markers and both CRP and GPx suggest that these parameters are promising prognostic factors in acute coronary syndromes.
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PMID:The relationship between trace elements and cardiac markers in acute coronary syndromes. 1596 72

Recent studies have demonstrated that electrical uncoupling at gap junctions during ischemia is associated with cardiac Connexin-43 (Cx43) dephosphorylation. Whether oxidative stress is involved in this phenomenon still remains unclear. In the present study, we examined the influence of selenium intake on reperfusion-induced Cx43 dephosphorylation. Male Wistar rats were fed a diet containing either 0.05 mg/kg (Low-Se, n = 13) or 1.5 mg/kg (High-Se, n = 11) selenium for 8 weeks. At the end of this diet, hearts were isolated and subjected to 10 min regional ischemia followed by 10 min reperfusion. The level of dephosphorylated Cx43 was determined in tissue samples from ischemic/reperfused and non-ischemic regions of the hearts. At the end of the experiemental diet, the activity of the antioxidant enzyme glutathione peroxidase (GSH-Px) was increased in high-Se hearts compared with low-Se hearts (+ 13%; p < 0.05). After ischemia/reperfusion, in low-Se hearts, Cx43 dephosphorylation appeared significantly increased in the left ventricle compared to the non-ischemic right ventricle (+ 149%; p < 0.05). The high-Se diet significantly reduced Cx43 dephosphorylation in the left ventricle (p < 0.05 vs. low-Se diet). In conclusion, our results suggest that oxidative stress may be involved in Cx43 dephosphorylation during myocardial ischemia/reperfusion, thereby contributing to arrhythmogenesis.
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PMID:Selenium status as determinant of connexin-43 dephosphorylation in ex vivo ischemic/reperfused rat myocardium. 1624 Jun 71

The aim of the present study was to investigate the protective effect of 1-(2,6-dimethylphenoxy)-2-(3,4-dimethoxyphenylethylamino) propane hydrochloride (DDPH) on myocardial ischemia-reperfusion (I/R) injury in rats and the mechanism of its myocardial protection. For this purpose, 50 Wistar rats were divided into five groups: sham group, control group, verapamil treated group, and two DDPH treated groups (20 and 40 mg/kg, respectively). Myocardial I/R injury model was established by reperfusion for 120 min after 40 min ischemia induced by the ligation of left descending coronary artery in rats. The influence of DDPH on myocardial infarction size was observed and the levels of myocardial enzymes in serum were measured. The activities of oxygen free radical scavenging enzymes and the content of malondialdehyde (MDA) in myocardium and serum were determined. The pathological changes of myocardial tissue were observed. The results showed that DDPH significantly diminished myocardial infarction size, reduced the release of myocardial creatine phosphokinase (CPK), lactate dehydrogenase (LDH) and glutamic oxaloacetic aminotransferase (GOT), protected the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and decreased the content of MDA in myocardium and serum as compared with the control group. The degree of myocardial injury was slighter in DDPH treated groups than in control group. These results suggest that DDPH produces a cardioprotective effect during myocardial I/R injury, which may be related to blocking calcium channels and inhibiting the formation of the oxygen free radical and subsequent peroxidation of lipid by DDPH.
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PMID:Protective effect of 1-(2,6-dimethylphenoxy)-2-(3,4-dimethoxyphenylethylamino) propane hydrochloride on myocardial ischemia-reperfusion injury in rats. 1639 71

The effects of chronic schisandrin B (Sch B) treatment (10 mg/kg/dayx15) on mitochondrial antioxidant status and sensitivity to Ca2+-induced permeability transition, as well as tissue heat shock protein (Hsp)25/70 production were examined in various tissues (brain, heart, liver, skeletal muscle) of young adult and middle-aged female rats. Age-dependent impairment in mitochondrial antioxidant status, as assessed by levels/activities of antioxidant components (reduced glutathione, alpha-tocopherol, Se-glutathione peroxidase and Mn-superoxide dismutase) and the extent of reactive oxygen species generation in vitro, was observed in brain, heart, liver and skeletal muscle tissues. While tissue Hsp25 levels remained relatively unchanged with aging, the Hsp70 level was increased in both brain and heart tissues of middle-aged rats. Chronic Sch B treatment was able to enhance mitochondrial antioxidant status and the resistance to Ca2+-induced mitochondrial permeability transition in an age-independent manner in various tissues of rats. However, Hsp25 and Hsp70 levels were only increased in young adult rats. The Sch B-induced enhancement of mitochondrial protective parameters in the heart was associated with the protection against myocardial ischemia-reperfusion injury in both young adult and middle-aged rats. The results suggest that chronic Sch B treatment may be beneficial for reversing the mitochondrial changes with aging and enhancing the heat shock response.
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PMID:Chronic schisandrin B treatment improves mitochondrial antioxidant status and tissue heat shock protein production in various tissues of young adult and middle-aged rats. 1662 87

Oxidative stress is associated with muscle fatigue and weakness in skeletal muscle of ischemic heart disease patients. Recently, it was found that endurance training elevates protective heat shock proteins (HSPs) and antioxidant enzymes in skeletal muscle in healthy subjects and antioxidant enzymes in heart failure patients. However, it is unknown whether coronary ischemia and mild infarct without heart failure contributes to impairment of stress proteins and whether exercise training reverses those effects. We tested the hypothesis that exercise training would reverse alterations in muscle TNF-alpha, oxidative stress, HSP70, SOD (Mn-SOD, Cu,Zn-SOD), glutathione peroxidase (GPX), and catalase (CAT) due to chronic coronary occlusion of the left circumflex (CCO). Yucatan swine were divided into three groups (n = 6 each): sedentary with CCO (SCO); 12 wk of treadmill exercise training following CCO (ECO); and sham surgery controls (sham). Forelimb muscle mass-to-body mass ratio decreased by 27% with SCO but recovered with ECO. Exercise training reduced muscle TNF-alpha and oxidative stress (4-hydroxynonenal adducts) caused by CCO. HSP70 levels decreased with CCO (-45%), but were higher with exercise training (+348%). Mn-SOD activity, Mn-SOD protein expression, and Cu,Zn-SOD activity levels were higher in ECO than SCO by 72, 82, and 112%, respectively. GPX activity was 177% greater in ECO than in SCO. CAT trended higher (P = 0.059) in ECO compared with SCO. These data indicate that exercise training following onset of coronary artery occlusion results in recovery of critical stress proteins and reduces oxidative stress.
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PMID:Exercise training reverses downregulation of HSP70 and antioxidant enzymes in porcine skeletal muscle after chronic coronary artery occlusion. 1687 55

Reactive oxygen species (ROS) enhance myocardial ischemia-reperfusion (I/R) injury. Ebselen, a seleno-organic glutathione peroxidase (GPx) mimetic, has a protective effect against tissue injury induced by ROS. However, the cardio-protective effect of orally administered ebselen has never been investigated in cardiac I/R injury. We investigated the effects and mechanisms of orally administered ebselen on experimental myocardial infarction. Isolated perfused rabbit hearts underwent 30 min of global ischemia and 60 min of reperfusion, with or without oral administration of ebselen 24 h before I/R, with or without enhanced oxidative stress by H202 infusion for the first 1 min of reperfusion. The recovery of left ventricular developed pressure (LVDP) was significantly improved, and the myocardial infarct size was significantly reduced by ebselen. The recovery of LVDP and the myocardial infarct size were markedly aggravated by H202 infusion. These enhancements by H202 were dose-dependently suppressed by ebselen, along with a reduction in myocardial 8-hydroxydeoxyguanosine levels, a marker for oxidative DNA damage. The myocardial reduced glutathione (GSH) level was preserved by ebselen. Ebselen markedly enhanced myocardial heat shock protein (HSP) 72 expression. The cardioprotective effect of ebselen-induced HSP72 was confirmed by MTT assay in isolated cardiomyocytes using KNK437, a novel HSP inhibitor. In conclusion, an oral administration of ebselen 24 h before I/R provided excellent cardioprotective effects, at least in part through HSP72 induction and GSH preservation.
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PMID:Oral pretreatment with ebselen enhances heat shock protein 72 expression and reduces myocardial infarct size. 1734 91

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