Research ExplorerPublicationsInhibition of xanthine oxidase improves myocardial contracti...

Inhibition of xanthine oxidase improves myocardial contractility in patients with ischemic cardiomyopathy.

Standard

Inhibition of xanthine oxidase improves myocardial contractility in patients with ischemic cardiomyopathy. / Baldus, Stephan; Müllerleile, Kai; Chumley, Phil; Steven, Daniel; Rudolph, Volker; Lund, Gunnar; Jürgen, Staude Hans; Stork, Alexander; Köster, Ralf; Kähler, Jan; Weiss, Christian; Münzel, Thomas; Meinertz, Thomas; Freeman, Bruce A; Heitzer, Thomas.

In: FREE RADICAL BIO MED, Vol. 41, No. 8, 8, 2006, p. 1282-1288.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Baldus, S, Müllerleile, K, Chumley, P, Steven, D, Rudolph, V, Lund, G, Jürgen, SH, Stork, A, Köster, R, Kähler, J, Weiss, C, Münzel, T, Meinertz, T, Freeman, BA & Heitzer, T 2006, 'Inhibition of xanthine oxidase improves myocardial contractility in patients with ischemic cardiomyopathy.', FREE RADICAL BIO MED, vol. 41, no. 8, 8, pp. 1282-1288. <http://www.ncbi.nlm.nih.gov/pubmed/17015175?dopt=Citation>

APA

Baldus, S., Müllerleile, K., Chumley, P., Steven, D., Rudolph, V., Lund, G., Jürgen, S. H., Stork, A., Köster, R., Kähler, J., Weiss, C., Münzel, T., Meinertz, T., Freeman, B. A., & Heitzer, T. (2006). Inhibition of xanthine oxidase improves myocardial contractility in patients with ischemic cardiomyopathy. FREE RADICAL BIO MED, 41(8), 1282-1288. [8]. http://www.ncbi.nlm.nih.gov/pubmed/17015175?dopt=Citation

Vancouver

Baldus S, Müllerleile K, Chumley P, Steven D, Rudolph V, Lund G et al. Inhibition of xanthine oxidase improves myocardial contractility in patients with ischemic cardiomyopathy. FREE RADICAL BIO MED. 2006;41(8):1282-1288. 8.

Bibtex

@article{826859553b47479abaf0cef1ccaed566,
title = "Inhibition of xanthine oxidase improves myocardial contractility in patients with ischemic cardiomyopathy.",
abstract = "Reactive oxygen species, in particular superoxide, have been closely linked to the underlying pathophysiology of ischemic cardiomyopathy: superoxide not only mediates mechanoenergetic uncoupling of the myocyte but also adversely impacts on myocardial perfusion by depleting endothelial-derived nitric oxide bioavailability. Xanthine oxidase generates superoxide upon oxidation of hypoxanthine and xanthine and has been detected in cardiac myocytes and coronary endothelial cells of patients with ischemic heart disease. Here we investigated the effects of oxypurinol, a xanthine oxidase inhibitor, on myocardial contractility in patients with ischemic cardiomyopathy. Twenty patients (19 males, 66+/-8 years) with stable coronary disease, severely suppressed systolic function (left ventricular ejection fraction 22+/-2%), and nonelevated uric acid plasma levels received a single intravenous dose of oxypurinol (400 mg). Cardiac MRI studies, performed before and 5.2+/-0.9 h after oxypurinol administration, revealed a reduction in end-systolic volumes (-9.7+/-4.2%; p=0.03) and an increase in left ventricular ejection fraction (+17.5+/-5.2%; p=0.003), whereas 6 patients (6 males, 63+/-3.8 years, ejection fraction 26+/-5%) who received vehicle only did not show significant changes in any of the parameters studied. Oxypurinol improves left ventricular function in patients with ischemic cardiomyopathy. These results underscore the significance of reactive oxygen species as important pathophysiological mediators in ischemic heart failure and point toward xanthine oxidase as an important source of reactive species that serve to modulate the myocardial redox state in this disease.",
author = "Stephan Baldus and Kai M{\"u}llerleile and Phil Chumley and Daniel Steven and Volker Rudolph and Gunnar Lund and J{\"u}rgen, {Staude Hans} and Alexander Stork and Ralf K{\"o}ster and Jan K{\"a}hler and Christian Weiss and Thomas M{\"u}nzel and Thomas Meinertz and Freeman, {Bruce A} and Thomas Heitzer",
year = "2006",
language = "Deutsch",
volume = "41",
pages = "1282--1288",
journal = "FREE RADICAL BIO MED",
issn = "0891-5849",
publisher = "Elsevier Inc.",
number = "8",

}

RIS

TY - JOUR

T1 - Inhibition of xanthine oxidase improves myocardial contractility in patients with ischemic cardiomyopathy.

AU - Baldus, Stephan

AU - Müllerleile, Kai

AU - Chumley, Phil

AU - Steven, Daniel

AU - Rudolph, Volker

AU - Lund, Gunnar

AU - Jürgen, Staude Hans

AU - Stork, Alexander

AU - Köster, Ralf

AU - Kähler, Jan

AU - Weiss, Christian

AU - Münzel, Thomas

AU - Meinertz, Thomas

AU - Freeman, Bruce A

AU - Heitzer, Thomas

PY - 2006

Y1 - 2006

N2 - Reactive oxygen species, in particular superoxide, have been closely linked to the underlying pathophysiology of ischemic cardiomyopathy: superoxide not only mediates mechanoenergetic uncoupling of the myocyte but also adversely impacts on myocardial perfusion by depleting endothelial-derived nitric oxide bioavailability. Xanthine oxidase generates superoxide upon oxidation of hypoxanthine and xanthine and has been detected in cardiac myocytes and coronary endothelial cells of patients with ischemic heart disease. Here we investigated the effects of oxypurinol, a xanthine oxidase inhibitor, on myocardial contractility in patients with ischemic cardiomyopathy. Twenty patients (19 males, 66+/-8 years) with stable coronary disease, severely suppressed systolic function (left ventricular ejection fraction 22+/-2%), and nonelevated uric acid plasma levels received a single intravenous dose of oxypurinol (400 mg). Cardiac MRI studies, performed before and 5.2+/-0.9 h after oxypurinol administration, revealed a reduction in end-systolic volumes (-9.7+/-4.2%; p=0.03) and an increase in left ventricular ejection fraction (+17.5+/-5.2%; p=0.003), whereas 6 patients (6 males, 63+/-3.8 years, ejection fraction 26+/-5%) who received vehicle only did not show significant changes in any of the parameters studied. Oxypurinol improves left ventricular function in patients with ischemic cardiomyopathy. These results underscore the significance of reactive oxygen species as important pathophysiological mediators in ischemic heart failure and point toward xanthine oxidase as an important source of reactive species that serve to modulate the myocardial redox state in this disease.

AB - Reactive oxygen species, in particular superoxide, have been closely linked to the underlying pathophysiology of ischemic cardiomyopathy: superoxide not only mediates mechanoenergetic uncoupling of the myocyte but also adversely impacts on myocardial perfusion by depleting endothelial-derived nitric oxide bioavailability. Xanthine oxidase generates superoxide upon oxidation of hypoxanthine and xanthine and has been detected in cardiac myocytes and coronary endothelial cells of patients with ischemic heart disease. Here we investigated the effects of oxypurinol, a xanthine oxidase inhibitor, on myocardial contractility in patients with ischemic cardiomyopathy. Twenty patients (19 males, 66+/-8 years) with stable coronary disease, severely suppressed systolic function (left ventricular ejection fraction 22+/-2%), and nonelevated uric acid plasma levels received a single intravenous dose of oxypurinol (400 mg). Cardiac MRI studies, performed before and 5.2+/-0.9 h after oxypurinol administration, revealed a reduction in end-systolic volumes (-9.7+/-4.2%; p=0.03) and an increase in left ventricular ejection fraction (+17.5+/-5.2%; p=0.003), whereas 6 patients (6 males, 63+/-3.8 years, ejection fraction 26+/-5%) who received vehicle only did not show significant changes in any of the parameters studied. Oxypurinol improves left ventricular function in patients with ischemic cardiomyopathy. These results underscore the significance of reactive oxygen species as important pathophysiological mediators in ischemic heart failure and point toward xanthine oxidase as an important source of reactive species that serve to modulate the myocardial redox state in this disease.

M3 - SCORING: Zeitschriftenaufsatz

VL - 41

SP - 1282

EP - 1288

JO - FREE RADICAL BIO MED

JF - FREE RADICAL BIO MED

SN - 0891-5849

IS - 8

M1 - 8

ER -