Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical studies have demonstrated that patients with coronary artery disease (CAD) have markers suggestive of increased free radical (FR) activity when compared with normal subjects; however, the relationship between the extent of CAD and level of FR markers is not known. The following indices of FR activity, plasma malondialdehyde (MDA), plasma thiols (PSH), red blood cell (RBC) glutathione (GSH), and RBC superoxide dismutase (SOD) were measured in 58 patients admitted for coronary angiography and in 50 matched controls. Regression analysis demonstrated no significant correlation between MDA, PSH, GSH, or SOD, and the angiographic grade which indicated the severity of the CAD. Patients with angiographically proven CAD (median 7.9 nmol/ml IQR 6.9-9.2) and patients with a history suggestive of angina pectoris but normal coronary angiograms (median 8.4 nmol/ml IQR 7.4-9.9) had significantly raised MDA levels compared with the controls (median 6.85 nmol/ml IQR 6.1-7.4), p less than 0.001 and p less than 0.005, respectively. The patients with angiographically proven CAD had significantly lower GSH levels (median 1461 microM IQR 1348-1709, p less than 0.002) compared with the controls (median 1754 microM IQR 1492-1930). Significantly raised SOD levels also were detected in patients with angiographically proven CAD (median 121.8 U/ml RBC, IQR 113.8-143.9) and in patients with a history of suggestive of angina pectoris but normal coronary angiograms (median 146 U/ml RBC, IQR 96.8-156.7) when compared with controls (median 96.3 U/ml RBC, IQR 82.4-115.6), p less than 0.001 and p less than 0.02, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relationship between the extent of coronary artery disease and indicators of free radical activity. 139 9

The changes of the plasma zinc, copper and erythrocyte glutathione peroxidase (GSH-Px) were measured by atomic absorption spectrometry and DTNB color development, in 31 patients suffering from coronary heart disease with angina Pectoris before and after taking Kuo-Guan granule one month. The results showed the plasma zinc was 16.83 +/- 2.60 mumol/L, copper 14.17 +/- 2.99 mumol/L, and erythrocyte GSH-Px 0.75 +/- 0.12 Eu/Hbmg/min in the normal control group. In patients with angina Pectoris, the plasma zinc was 14.39 +/- 4.44 mumol/L, copper 17.47 +/- 4.42 mumol/L, and erythrocyte GSH-Px 0.49 +/- 0.075 Eu/Hbmg/min before treatment; the plasma zinc was 20.17 +/- 3.97 mumol/L, copper 15.74 +/- 3.15 mumol/L, and erythrocyte GSH-Px 0.72 +/- 0.10 Eu/Hbmg/min after treatment. These results indicate that the plasma zinc and erythrocyte GSH-Px were lower and copper was higher in the patients than the normal control group before treatment (P less than 0.01), the plasma zinc and erythrocyte GSH-Px were increased and copper was decreased after treatment (P less than 0.01). These suggest that therapeutic mechanism of Kuo-Guan granule to coronary heart disease with angina Pectoris may be related to it's regulation on trace elements disturbance in body.
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PMID:[Effects of kuo-guan granule on plasma zinc, copper and erythrocyte GSH-Px (glutathione peroxidase) in patients with angina pectoris]. 239 54

The effect of Sheng Mai San (SMS) on the coronary heart disease (CHD) patients (30 angina pectoris and 68 acute myocardial infarction, AMI) and its peroxidation damage was studied. It was shown that the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in blood were decreased and the content of malondialdehyde (MDA) in plasma was increased in CHD patients in comparison with the healthy controls (P < 0.001). When SMS was orally administered in 38 AMI patients, both SOD and GSH-Px activities were increased and the level of MDA decreased (P < 0.05), and these changes were even more significant when SMS was further ingested for another two weeks (P < 0.001). At the same time, it was found that the changes of SOD, GSH-Px and MDA in the control group (30 AMI patients not taking SMS) were not significantly different (P > 0.05). It could be assumed that the pathogenesis of CHD is associated with free radical (FR) triggering a chain reaction of the lipid peroxidation, and that SMS is acting as an effective free radical scavenger, which would ameliorate the lipid peroxidation damage. Thus, SMS could be administered in the prevention and the treatment of CHD.
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PMID:[Effect of sheng mai san on lipid peroxidation in acute myocardial infarction patients]. 771 2

The aim of this study was to determine whether oxidative stress occurs in unstable angina. Thirty patients with unstable angina class B (Braunwald classification) were prospectively studied. Control groups consisted of 23 patients presenting with stable angina and of 21 age-matched healthy volunteers. Upon admission and every 8 h for 24 h, blood samples were drawn for the determination of plasma malondialdehyde (MDA) levels, Se-glutathione peroxidase (GPX) activity, erythrocyte reduced glutathione (GSH) concentrations, erythrocyte GPX and superoxide dismutase (SOD) activities. Coronary angiograms were performed within 4 days of admission in 26 out of the 30 patients included in the study. Nine of these 30 patients were subsequently identified as presenting a non-Q wave myocardial infarction and were separately examined. On admission, only plasma MDA levels and erythrocyte GSH concentrations differed among groups. Plasma MDA levels of patients presenting with unstable angina (P < 0.01) and acute myocardial infarction (P < 0.05) were higher than those of patients with stable angina and of normal volunteers, whereas there was no difference in these parameters between unstable angina and non-Q wave myocardial infarction groups. Erythrocyte GSH concentration was lower in all patient groups as compared to normal subjects. ANOVA for repeated measures showed no difference between admission and subsequent levels for all parameters. Finally, no difference was observed for any of the parameters when anti-ischaemic or anti-aggregant treatment before admission, or the number of affected vessels on coronary angiograms, were considered. We conclude that an oxidative stress can be evidenced in patients with unstable angina or acute myocardial infarction.
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PMID:Oxidative stress in patients with unstable angina. 800 17

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

The pharmacological action of glyceryl trinitrate (GTN), a widely used drug for the treatment of angina pectoris, is thought to be mediated through release of nitric oxide (NO) during its biotransformation. Since glutathione S-transferases (GST) can utilize GTN as substrate and GST inhibitors can attenuate GTN-induced relaxation of rabbit aorta in vitro it has been suggested that these enzymes are involved in the bioactivation of GTN in rabbit aorta. Because GSTs are multifunctional enzymes and a multitude of GST isozymes with varying substrate preferences are present in mammalian tissues, the role of specific GST isozymes in bioactivation of GTN in rabbit aorta needs to be established. Therefore, during the present studies we have purified and characterized GST isozymes from rabbit aorta and evaluated their possible roles in the biotransformation of GTN. The results of these studies showed that rabbit aorta contained three GST isozymes having pI values of 9.4, 7.7, and 5.4. Structural, immunological, and kinetic studies showed that GST 9.4, GST 7.7, and GST 5.4 belonged to the alpha-, pi-, and mu-classes, respectively. The relative abundance of these enzymes in rabbit aorta was alpha > pi > mu. The alpha- and mu-class GST isozymes had similar activities toward GTN (0.71 U/mg and 0.86 U/mg, respectively) while the pi-class GST showed much lower activity toward GTN. The catalytic efficiency k(cat)/Km of the mu- and alpha-class GSTs toward GTN were similar but these activities were differentially inhibited by ethacrynic acid, its GSH conjugate, bromosulfophthalein (BSP), and hematin. These results suggest that in rabbit aorta GSTs may be involved in bioactivation of GTN, and because of their higher abundance the alpha-class GSTs may be more important for the pharmacological effects of GTN than the mu-class GSTs. The results on kinetics of inhibition by various inhibitors suggest that hematin may be an effective inhibitor to delineate the role of specific GST isozymes in the bioactivation of GTN.
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PMID:Rabbit aorta glutathione S-transferases and their role in bioactivation of trinitroglycerin. 888 55

This study examined the effect of reduced glutathione (GSH), an important antioxidant that restores intracellular redox imbalance and prevents inactivation of endothelial-derived nitric oxide, on the abnormal vasomotor reactivity in spastic coronary arteries. The responses of epicardial diameter of the left coronary arteries to intracoronary infusion of acetylcholine (ACh; 50 microg/min) were measured by quantitative coronary angiography before and during combined intracoronary infusion of GSH (50 mg/min for 6 min) or saline as a placebo in 24 patients with coronary spastic angina and in 28 control patients. All of the spastic coronary arteries showed constrictor response to ACh, whereas the control coronary arteries as a whole showed only minimal diameter changes to ACh. GSH infusion suppressed constrictor response of epicardial diameter to ACh in patients with coronary spastic angina, whereas it had no significant effect in control subjects. Saline infusion did not have any effects. The results indicate that GSH attenuated the constrictor response to ACh in epicardial coronary arteries of patients with coronary spastic angina. GSH may have an important role in the regulation of coronary vasomotor function in patients with coronary spastic angina.
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PMID:Glutathione attenuates coronary constriction to acetylcholine in patients with coronary spastic angina. 1112 41

Effects of amino acid composition MP-33 in combination with trimetazidine were studied in metabolic therapy of elderly patients (age 63.3 +/- 1.7 years) with ischemic heart disease (angina pectoris functional class II-III). MP-33 (100 mg 3 times a day subling.), trimetazidine (20 mg 3 times a day per os), trimetazidine + amino acid composition MP-33 in the above doses in addition to basic therapy were given to 30, 15 and 15 patients, respectively. Combined therapy with trimetazidine and MP-33 significantly activated antioxidant enzymes and depressed lipid peroxidation due to GSH-dependent regulation of cellular redox status by MP-33.
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PMID:[Enhancement of antioxidant status of the elderly patients with ischemic heart disease in response to amino acid composition of MP-33 in combined therapy with trimetazidine]. 1208 89

The effect of fluvastatin and fenofibrate on antioxidative enzymatic activity in patients with stable angina and mixed hyperlipidaemia was investigated. Thirty-five patients (13 men and 22 women) aged 40-77 years, were randomly divided into two groups. The first group comprised 20 patients who were administered fluvastatin 40 mg once daily at bedtime for 30 days. The second group consisted of 15 patients who were administered fenofibrate 200 mg once daily at bedtime for 30 days. The control group comprised 11 clinically healthy persons aged 21-54 years. The activities of SOD-1, CAT and GSH-Px in erythrocytes were measured. Fluvastatin induced an increase of the activities of all investigated enzymes. Fenofibrate caused no change of enzyme activities in patients with dyslipidaemia.
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PMID:[Effect of fluvastatin and fenofibrate on the antioxidative barrier enzyme activity in patients with dyslipidemia]. 1286 85

Effect of carvedilol on the antioxidative enzymatic defence was investigated in patients with stable angina. The study comprised 27 patients (20 men and 10 women), aged 38-55 years (mean 48.3 years) with stable angina. The patients were administered carvedilol in increasing every four weeks doses: 12.5 mg/day, 25 mg/day, 50 mg/day. The control group consisted of 12 healthy subjects aged 39-49 years (mean 45.7 years). Blood samples were collected before and 4, 8 and after 12 weeks of therapy in patients and once in control group. Our study has been approved by the local Ethics Committee. Superoxide dismutase (SOD-1), glutathione peroxidase (GSH-Px) and catalase (CAT) activities in erythrocytes were determined according to Misra and Fridovich, Little and O'Brien and Beers and Sizer; respectively. The enzymatic antioxidative defence was significantly decreased in patients with stable angina in comparison to healthy subjects. During carvedilol therapy an increase in SOD-1, GSH-Px and CAT activities was observed. Moreover GSH-Px activity after 8 and 12 weeks of carvedilol therapy did not differ from that observed in group of healthy subjects. The results of our study have shown that carvedilol enhances antioxidative enzymatic defence in patients with stable angina.
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PMID:[Effect of carvedilol on antioxidative enzymatic defence in patients with stable angina]. 1787 21


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