Oxy free radical system in heart failure and therapeutic role of oral vitamin E

Ghatak, Ashim; Brar, Mohan Jeet Singh; Agarwal, Ajay; Goel, Neena; Rastogi, Anil K.; Vaish, Arvind Kumar; Sircar, A. R.; Chandra, M.

doi:10.1016/s0167-5273(96)02787-8

Cited by 105 publications

(57 citation statements)

References 22 publications

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“…Antioxidants, such as SOD and catalase, are reportedly decreased in patients with heart failure, 5 but in the present study, the serum TRX levels in patients with NYHA functional class III or IV, were significantly elevated. We postulate that the increase in the serum concentration of TRX may indirectly reflect the excessive oxidative stress caused by ROS associated with uncontrolled heart failure.…”

Section: Discussioncontrasting

confidence: 82%

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Serum Thioredoxin (TRX) Levels in Patients With Heart Failure

Kishimoto

Shioji²,

Nakamura

et al. 2001

Jpn Circ J

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Section: Discussioncontrasting

confidence: 82%

“…5,10 There is an increase in lipid peroxides in the blood of patients with congestive heart failure, and a significant negative correlation with LVEF. 6 ROS may exacerbate ischemiainduced injury by promoting unfavorable oxidative changes in membrane lipids and ion pumps, which causes reperfusion-induced arrhythmia.…”

Section: Discussionmentioning

confidence: 99%

Serum Thioredoxin (TRX) Levels in Patients With Heart Failure

Kishimoto

Shioji²,

Nakamura

et al. 2001

Jpn Circ J

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“…1 This complex clinical syndrome is associated with a wide spectrum of abnormalities including endothelial dysfunction and increased oxidative stress. [2][3][4][5][6] …”

mentioning

confidence: 99%

Allopurinol Improves Endothelial Dysfunction in Chronic Heart Failure

et al. 2002

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Background-Increased oxidative stress in chronic heart failure is thought to contribute to endothelial dysfunction.Xanthine oxidase produces oxidative stress and therefore we examined whether allopurinol improved endothelial dysfunction in chronic heart failure. Methods and Results-We performed a randomized, placebo-controlled, double-blind crossover study on 11 patients with New York Heart Association class II-III chronic heart failure, comparing 300 mg allopurinol daily (1 month) versus placebo. Endothelial function was assessed by standard forearm venous occlusion plethysmography with acetylcholine, nitroprusside, and verapamil. Plasma malondialdehyde levels were also compared to assess significant changes in oxidative stress. Allopurinol significantly increased the forearm blood flow response to acetylcholine (percentage change in forearm blood flow [meanϮSEM]: 181Ϯ19% versus 120Ϯ22% allopurinol versus placebo; Pϭ0.003). There were no significant differences in the forearm blood flow changes between the placebo and allopurinol treatment arms with regard to sodium nitroprusside or verapamil. Plasma malondialdehyde was significantly reduced with allopurinol treatment (346Ϯ128 nmol/L versus 461Ϯ101 nmol/L, allopurinol versus placebo; Pϭ0.03), consistent with reduced oxidative stress with allopurinol therapy. Conclusions-We have shown that allopurinol improves endothelial dysfunction in chronic heart failure. This raises the distinct possibility that allopurinol might reduce cardiovascular events and even improve exercise capacity in chronic heart failure.

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“…9 Xanthine oxidase (XO), an enzyme that forms ⅐ O 2 -in the catalysis of the terminal steps in purine metabolism, has been implicated as a pathogenic factor in heart failure and reperfusion injury. 13,14 XO is a molybdenum-containing enzyme found both in the cytoplasm and bound to the plasma membrane of endothelial cells, 15 as well as circulating in the plasma. 16,17 In most mammals, including humans, XO activity is found primarily in the liver and intestine, from which it may be released into the circulation and affect remote organs such as the heart.…”

mentioning

confidence: 99%

Intravenous Allopurinol Decreases Myocardial Oxygen Consumption and Increases Mechanical Efficiency in Dogs With Pacing-Induced Heart Failure

Ekelund

Harrison

Shokek

et al. 1999

Circulation Research

214

163

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Abstract-Allopurinol, an inhibitor of xanthine oxidase, increases myofilament calcium responsiveness and blunts calcium cycling in isolated cardiac muscle. We sought to extend these observations to conscious dogs with and without pacing-induced heart failure and tested the prediction that allopurinol would have a positive inotropic effect without increasing energy expenditure, thereby increasing mechanical efficiency. In control dogs (nϭ10), allopurinol (200 mg IV) caused a small positive inotropic effect; (dP/dt) max increased from 3103Ϯ162 to 3373Ϯ225 mm Hg/s (ϩ8.3Ϯ3.2%; Pϭ0.01), but preload-recruitable stroke work and ventricular elastance did not change. In heart failure (nϭ5), this effect was larger; (dP/dt) max rose from 1602Ϯ190 to 1988Ϯ251 mm Hg/s (ϩ24.4Ϯ8.7%; Pϭ0.03), preload-recruitable stroke work increased from 55.8Ϯ9.1 to 84.9Ϯ12.2 mm Hg (ϩ28.1Ϯ5.3%; Pϭ0.02), and ventricular elastance rose from 6.0Ϯ1.6 to 10.5Ϯ2.2 mm Hg/mm (Pϭ0.03). Allopurinol did not affect myocardial lusitropic properties either in control or heart failure dogs. In heart failure dogs, but not controls, allopurinol decreased myocardial oxygen consumption (-49Ϯ4.6%; Pϭ0.002) and substantially increased mechanical efficiency (stroke work/myocardial oxygen consumption; ϩ122Ϯ42%; Pϭ0.04). Moreover, xanthine oxidase activity was Ϸ4-fold increased in failing versus control dog hearts (387Ϯ125 versus 78Ϯ72 pmol/min ⅐ mg -1 ; Pϭ0.04) but was not detectable in plasma. These data indicate that allopurinol possesses unique inotropic properties, increasing myocardial contractility while simultaneously reducing cardiac energy requirements. The resultant boost in myocardial contractile efficiency may prove beneficial in the treatment of congestive heart failure. (Circ Res. 1999;85:437-445.)

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Oxy free radical system in heart failure and therapeutic role of oral vitamin E

Cited by 105 publications

References 22 publications

Serum Thioredoxin (TRX) Levels in Patients With Heart Failure

Serum Thioredoxin (TRX) Levels in Patients With Heart Failure

Allopurinol Improves Endothelial Dysfunction in Chronic Heart Failure

Intravenous Allopurinol Decreases Myocardial Oxygen Consumption and Increases Mechanical Efficiency in Dogs With Pacing-Induced Heart Failure

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