Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The fibrinolytic activity of blood has a circadian variation with increased thrombotic tendency in the morning. This may be a contributory factor to the circadian variation in the time of onset of thrombotic events. However, there has recently been increasing interest to the role of the white blood cells (WBC) and free radicals (FRs) in thrombosis. We have previously reported a circadian variation in WBC aggregation and FR status in normal volunteers. No one has yet studied possible circadian variations in these parameters in patients with stable ischaemic heart disease (IHD). Ten men with stable IHD had blood samples collected at four-hourly intervals from midday until midday the following day. The patients were ambulant until midnight at which time they went to bed and remained in bed until 0800 h. The following were measured on each sample: WBC aggregation, malondialdehyde (MDA) which is a product of lipid peroxidation by FRs; the FR scavengers, plasma thiol (PSH), red cell glutathione (GSH) and superoxide dismutase (SOD) which are all altered in the presence of increased FR activity. WBC aggregation and PSH had significant circadian variations, P < 0.015 and P < 0.001 respectively. The WBC aggregation peak was at 1200 h and trough at 1600 h, the PSH peak was at midnight and the trough at 0400 h. WBC behaviour and FR status influence the flow properties of blood. The largest rise in WBC aggregation occurred from 0800 h to 1200 h; such an increase in aggregation could predispose to microcirculatory occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Circadian variation of white blood cell aggregation and free radical indices in men with ischaemic heart disease. 128 92

Tocopherols and tocotrienols (vitamin E) and ascorbic acid (vitamin C) as well as the carotenoids react with free radicals, notably peroxyl radicals, and with singlet molecular oxygen (1O2), this being the basis of their function as antioxidants. RRR-alpha-tocopherol is the major peroxyl radical scavenger in biological lipid phases such as membranes or low-density lipoproteins (LDL). L-Ascorbate is present in aqueous compartments (e.g. cytosol, plasma, and other body fluids) and can reduce the tocopheroxyl radical; it also has a number of metabolically important cofactor functions in enzyme reactions, notably hydroxylations. Upon oxidation, these micronutrients need to be regenerated in the biological setting, hence the need for further coupling to nonradical reducing systems such as glutathione/glutathione disulfide, dihydrolipoate/lipoate, or NADPH/NADP+ and NADH/NAD+. Carotenoids, notably beta-carotene and lycopene as well as oxycarotenoids (e.g. zeaxanthin and lutein), exert antioxidant functions in lipid phases by free-radical or 1O2 quenching. There are pronounced differences in tissue carotenoid patterns, extending also to the distribution between the all-trans and various cis isomers of the respective carotenoids. Antioxidant functions are associated with lowering DNA damage, malignant transformation, and other parameters of cell damage in vitro as well as epidemiologically with lowered incidence of certain types of cancer and degenerative diseases, such as ischemic heart disease and cataract. They are of importance in the process of aging. Reactive oxygen species occur in tissues and cells and can damage DNA, proteins, carbohydrates, and lipids. These potentially deleterious reactions are controlled in part by antioxidants that eliminate prooxidants and scavenge free radicals. Their ability as antioxidants to quench radicals and 1O2 may explain some anticancer properties of the carotenoids independent of their provitamin A activity, but other functions may play a role as well. Tocopherols are the most abundant and efficient scavengers of peroxyl radicals in biological membranes. The water-soluble antioxidant vitamin C can reduce tocopheroxyl radicals directly or indirectly and thus support the antioxidant activity of vitamin E; such functions can be performed also by other appropriate reducing compounds such as glutathione (GSH) or dihydrolipoate. The biological efficacy of the antioxidants is also determined by their biokinetics.
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PMID:Antioxidant functions of vitamins. Vitamins E and C, beta-carotene, and other carotenoids. 144 60

In the isolated and perfused rabbit heart ischemia induced a rapid decline of contractility, associated with a reduction of the content of tissue GSH with no significant changes in GSSG. Reperfusion induced a small recovery of contractility, a substantial release of total glutathione and a further decrease in the content of tissue GSH with a significant increase of tissue GSSG. Glutathione reductase and glutathione peroxidase activities were not affected by ischemia and reperfusion. This study suggests a possible role for glutathione in the determination of functional damage induced by myocardial ischemia and reperfusion.
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PMID:Changes in the cardiac glutathione status after ischemia and reperfusion. 396 36

Protective effects of a perfluorooctylbromide emulsion on myocardial ischemia and reperfusion (MI/R) injury were evaluated in a modified Langendorff rat heart preparation. Isolated rat hearts were equilibrated in Krebs-Henseleit solution (KH) for 35 minutes and perfused with either cardioplegic solution (CPS) or a 100% perfluorooctylbromide (PFOB) emulsion in CPS for 3 minutes. Hearts were then bathed in the emulsion or CPS. Both groups were subjected to 30 minutes of ischemia. Following 30 minutes of ischemia and 30 minutes of reperfusion with KH solution, hearts subjected to the 100% PFOB emulsion showed improved recovery of left ventricular function. Tissue activities of the antioxidant enzymes glutathione peroxidase, superoxide dismutase, and catalase were not affected by the emulsion in this model. Activity of lactate dehydrogenase (LDH) in the bathing medium was elevated at the end of the experimental period in both control and PFOB-treated hearts. The PFOB emulsion reduced the decline in ATP and GSH levels produced by cardioplegia and subsequent reperfusion. No differences were noted in oxidized glutathione (GSSG) levels. These data suggest that the PFOB emulsion provides some protection for the myocardium against injury associated with cardioplegia.
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PMID:Effects of a 100% perfluorooctylbromide emulsion on ischemia/reperfusion injury following cardioplegia. 758 37

Vascular endothelium is one of the first tissues exposed to reactive oxygen species produced during myocardial ischemia-reperfusion. Bovine coronary venular endothelial cells (CVEC) were evaluated for intracellular glutathione (GSH) levels and heat shock protein 70 (HSP 70) mRNA and protein during in vitro oxidative stress. CVEC were incubated with 0.01875 U/ml xanthine oxidase (XO) and 0.5 mM hypoxanthine (HX) for 30 min and then allowed to recover for 0, 1, 2, or 3 h. Relative GSH levels were determined by evaluation of monochlorobimane fluorescence. GSH fluorescence was significantly lower in CVEC treated with XO+HX for 30 min than in controls. GSH fluorescence was also decreased in heat-shocked CVEC. After oxidative stress, GSH levels were higher than in controls at 1 h, but by 2 or 3 h after treatment, GSH fluorescence fell below control values. HSP 70 mRNA was induced in CVEC by a 30-min treatment with XO+HX exposure. These data suggest that CVEC respond to oxidative stress by reducing intracellular GSH levels and inducing HSP 70 mRNA, although significant increases in HSP 70 protein were not detected at the time points tested.
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PMID:Oxidative injury of coronary venular endothelial cells depletes intracellular glutathione and induces HSP 70 mRNA. 773 67

During exercise there is an increase of oxygen consumption with production of superoxide anion. Tocopherols and ubiquinones are intrinsic lipid components involved in antioxidant protection and also glutathione reduced is an important water soluble antioxidant. The authors take into consideration 28 patients with ischemic heart disease coming in a rehabilitation center. In a group of 14 of them we studied the effects on the exercise ergonometer test of administration of 1200 mg of tocopherol on the behaviour of ubiquinone plasmatic levels and GSH. In this group CoQ10 after exercise increase significantly (0.762 SD 0.134 g/ml before vs 0.827 SD 0.89 after). GSH doesn't increase after (2.5 SD 0.459 mM/l vs 2.492 SD 0.457). In the group of patients without tocopherol after exercise CoQ10 decrease significantly (-39%) and also GSH has the same behaviour (-15%). Our study shows that the administration of tocopherol prevents lipoperoxidation occurring during exercise test.
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PMID:[CoQ10 blood levels and erythrocyte concentration of GSH in ischemic heart patients during exercise test (effects of vitamin E)]. 779 18

Effect of myocardial ischaemia on the bioantioxidants levels in the cat heart was evaluated. In addition, effect of curcumin, an anti-inflammatory and anti-thrombotic drug, and quinidine, a standard antiarrhythmic drug, was also studied in the cat. Myocardial ischaemia was induced by the ligation of left descending coronary artery. Quinidine (1 mg/kg, iv) was administered 15 min prior to while curcumin (100 mg/kg, ip) was given 30 min before ligation. Hearts were removed 4 h post coronary artery ligation. Levels of glutathione (GSH), malonaldelhyde (MDA), myeloperoxidase (MPO), superoxide dismutase (SOD), catalase (CAT) and lactate dehydrogenase (LDH) were estimated in the ischaemic and non-ischaemic zones. Both the drugs protected the animals against decrease in the heart rate and blood pressure following ischaemia. In the ischaemic zone, after 4 h of ligation, an increase in the level of MDA and activities of MPO and SOD (cytosolic fraction) were observed. Quinidine and curcumin pretreatment prevented the ischaemia-induced elevation in MDA contents and LDH release. Curcumin pretreatment did not prevent the increase in MPO activity while quinidine did. Results obtained indicate alterations in the bioantioxidants following ischaemia and both curcumin and quinidine prevented ischaemia induced changes in the cat heart.
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PMID:Prevention of ischaemia-induced biochemical changes by curcumin & quinidine in the cat heart. 788 81

This study was performed to observe the effect of myocardial ischemia on the patients undergoing cardiopulmonary bypass (CPB) operation. For this aim, superoxide dismutase (SOD) activities, reduced glutathione (GSH) and lipid peroxide (LP) levels were determined in blood samples which were obtained from the coronary sinus. Sampling times were as follows: (1) Before CPB. (2) Immediately after CPB. (3) Fifteen minutes after the second specimen. (4) Thirty minutes after the second specimen. SOD activities of these groups were 5135.10 +/- 278.51 U/g Hb, 3505.64 +/- 302.09 U/g Hb, 4206.55 +/- 272.25 U/g Hb, 4707.20 +/- 270.91 U/g Hb respectively. Also the LP levels were 1.90 +/- 0.29 nmol MDA/ml, 4.37 +/- 0.52 nmol MDA/ml, 4.09 +/- 0.39 nmol MDA/ml, 2.74 +/- 0.30 nmol MDA/ml respectively. GSH levels were slightly increased during ischemia and reperfusion; 103.27 +/- 5.18 mg/dl, 125.00 +/- 10.36 mg/dl, 125.00 +/- 6.61 mg/dl, 111.18 +/- 8.22 mg/dl respectively. SOD activities were reduced significantly in second group (p < 0.001), in third and fourth groups (p < 0.01) as compared with control group. Also LP levels were increased significantly in all groups (p < 0.001) as compared with controls. Our results confirm the generation of oxygen free radicals from ischemia and reperfusion of heart during CPB. Also it appears that oxygen free radical generation exceeds the capacity of intracellular SOD, which is the most important scavenger of free radical in the cell.
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PMID:Oxygen free radicals in erythrocytes during open heart operation. 819 75

Selenium concentration in blood, glutathionperoxidase (GSH-Px) activity in erythrocytes and lipid peroxides in plasma were studied in patients with ischemic heart disease, hypertrophic (HCMP) and dilated cardiomyopathy (DCMP). Patients with IHD, HCMP and DCMP revealed depressed activity of GSH-Px with activation of lipid peroxides associated with lowered selenium content in blood. The selenium content in blood was lower in patients with severe forms of IHD Daily intake of 300 micrograms selenium with "Selena" during a month increases selenium concentration by 71% in patients with IHD and DCMP. This increase change inversely with primary selenium concentration in plasma. Plasma Malone dialdehyde concentration decreased by 17%. The results obtained suggest participation of selenium in cardiomyopathy and IHD pathogenesis, thus forming a basis for selecting the patients with selenium deficiency for its further correction with "Selena."
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PMID:[The clinical significance of selenium deficiency in patients from the Samara region with cardiovascular diseases and its correction with the preparation Selena]. 870 83

Organic nitrates are widely used in the treatment of ischemic heart disease. The magnitude and duration of their circulatory and ischemic effects are, however, rapidly reduced during continuous treatment. The specific mechanisms underlying this tolerance development are not clear. According to the most widely accepted theory, tolerance is due to an intracellular depletion of thiol compounds (GSH and/or cysteine) involved in the conversion of nitrates to vasoactive intermediates. This presentation deals with aspects of in vivo thiol/nitrate interactions in different experimental and clinical conditions. The major results and conclusions are: The acute hypotensive effect of NTG is decreased by lowering of intracellular GSH levels. This finding emphasizes that normal intracellular thiol levels are required for optimal conversion of nitrates. Thus, intracellular GSH plays a critical role in the metabolism of NTG. Despite development of tolerance to the hypotensive effect of NTG, arterial and venous thiol levels are similar in nitrate tolerant and non-tolerant animals, suggesting that depletion of vascular thiol compounds may not be the cause of nitrate tolerance in vivo. The effect of exogenous thiol administration on intravascular thiol levels are different in nitrate tolerant and non-tolerant conscious rats. Exogenous thiol compounds (e.g. NAC) augments the hypotensive effect of NTG by a tolerance nonspecific mechanism. This effect is most likely mediated by an extracellular and/or membrane-related nitrate/thiol interaction and formation of NO. N-acetylcysteine inhibits angiotensin converting enzyme and counteracts nitrate-induced stimulation of the renin angiotensin system in vivo. Therefore, in addition to an effect on nitrate metabolism, thiol compounds may modify tolerance development by attenuating nitrate-induced counter-regulatory mechanisms. In the clinical setting, co-administration of NAC and ISDN delays and partially prevents tolerance to the antianginal and antiischemic effects normally seen in patients with stable angina pectoris during treatment with ISDN. N-acetylcysteine treatment in humans, potentiates and preserves nitrate induced venodilation and augments the effect of nitrates on small resistance vessels without affecting the response to nitrates in larger sized arteries. Thus, administration of NAC may change the normal vasodilator profile of nitrates. In conclusion, changes in cellular thiol levels may modify the hemodynamic effect of organic nitrates and the cellular handling of thiols and/or thiol related enzymes is altered after development of nitrate tolerance. In addition, a tolerance unrelated thiol/nitrate interaction, potentiating the effect of nitrates, may occur after administration of exogenous thiol compounds. In the clinical setting administration of thiols results in a characteristic change in the vasodilator profile of nitrates and an attenuation of the nitrate-induced stimulation of the renin-angiotensin system. The combination of these effects probably contributes to the improvement in antianginal and antiischemic parameters which may be seen during continuous and prolonged treatment with nitrates and thiol compounds.
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PMID:Thiol compounds and organic nitrates. 874 3


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