EVIDENCE OF OXIDATIVE STRESS IN CHRONIC HEART-FAILURE IN HUMANS

被引:218
作者
MCMURRAY, J
CHOPRA, M
ABDULLAH, I
SMITH, WE
DARGIE, HJ
机构
[1] WESTERN INFIRM & ASSOCIATED HOSP,DEPT CARDIOL,GLASGOW G11 6NT,SCOTLAND
[2] UNIV STRATHCLYDE,DEPT CHEM,GLASGOW G1 1XW,SCOTLAND
关键词
OXIDATIVE STRESS; FREE RADICALS; CHRONIC HEART FAILURE; GLUTATHIONE; SUPEROXIDE DISMUTASE; LIPID PEROXIDATION;
D O I
10.1093/eurheartj/14.11.1493
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Chronic heart failure (CHF) due to coronary artery disease (CAD) has been shown to be associated with increased plasma thiobarbituric reactive substances (TEARS) and reduced plasma thiol (PSH) concentrations, suggesting oxidative stress (OS). The aims of the present studies were (a) to determine whether OS is due to CAD or CHF per se and (b) to determine if a wider range of more specific markers of OS are 'abnormal in CHF. In the first study, two groups of patients (n=15 each) were compared. Group 1 (11 male, mean age 56 years) had CHF due to CAD and group 2 (12 male, mean age 53 years) had non-CAD CHF. Median plasma TEARS in controls was 7.6 nmol . ml-1, 10.0 nmol . ml-1 in group 1 and 9.3 nmol . ml-1 in group 2 (P<0.01 both groups vs control). Median PSH was 505 384 and 364 nmol . ml-1 (P<0.05 and P<0.01 vs control) respectively. Fifty-three patients with CHF were recruited in the second study. Malondialdehyde and PSH were 10.3 and 409 nmol . ml-1 respectively, compared to control values of 7.9 and 560 nmol . ml-1 (both P<0.001). The median values for the following additional measures of OS in controls and patients were: erythrocyte superoxide dismustase 131 vs 114 U . l-1 (P=0.005); caendoplasmin oxidase 97 vs 197 U . l-1 (P<0.01); erythrocyte glutathione 1.56 nmol . ml-1 vs 1.77 nmol . ml-1 (P<0.02); plasma conjugated dienes 0.28 vs 0.33 optical density units (P=ns). Chronic heart failure, regardless of aetiology, is associated with abnormalities of a range of markers of OS. © 1993 The European Society of Cardiology.
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页码:1493 / 1498
页数:6
相关论文
共 48 条
  • [1] AUST SD, 1988, HDB METHODS OXYGEN R
  • [2] FREE-RADICAL PATHOLOGY IN CHRONIC ARTERIAL-DISEASE
    BELCH, JJF
    CHOPRA, M
    HUTCHISON, S
    LORIMER, R
    STURROCK, RD
    FORBES, CD
    SMITH, WE
    [J]. FREE RADICAL BIOLOGY AND MEDICINE, 1989, 6 (04) : 375 - 378
  • [3] BELCH JJF, 1991, BRIT HEART J, V65, P245
  • [4] MARKED REDUCTION OF FREE-RADICAL GENERATION AND CONTRACTILE DYSFUNCTION BY ANTIOXIDANT THERAPY BEGUN AT THE TIME OF REPERFUSION - EVIDENCE THAT MYOCARDIAL STUNNING IS A MANIFESTATION OF REPERFUSION INJURY
    BOLLI, R
    JEROUDI, MO
    PATEL, BS
    ARUOMA, OI
    HALLIWELL, B
    LAI, EK
    MCCAY, PB
    [J]. CIRCULATION RESEARCH, 1989, 65 (03) : 607 - 622
  • [5] BROTTMAN MD, 1990, CIRCULATION, V82, P316
  • [6] BURRELL CJ, 1989, BRIT HEART J, V61, P4
  • [7] CHEN X, 1986, ACTA PHARMACOL TOX, V59, P325
  • [8] AUGMENTATION OF PLASMA NOR-EPINEPHRINE RESPONSE TO EXERCISE IN PATIENTS WITH CONGESTIVE HEART FAILURE
    CHIDSEY, CA
    BRAUNWALD, E
    HARRISON, DC
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1962, 267 (13) : 650 - &
  • [9] CAPTOPRIL - A FREE-RADICAL SCAVENGER
    CHOPRA, M
    SCOTT, N
    MCMURRAY, J
    MCLAY, J
    BRIDGES, A
    SMITH, WE
    BELCH, JJF
    [J]. BRITISH JOURNAL OF CLINICAL PHARMACOLOGY, 1989, 27 (03) : 396 - 399
  • [10] FREE-RADICAL ACTIVITY IN TYPE-2 DIABETES
    COLLIER, A
    WILSON, R
    BRADLEY, H
    THOMSON, JA
    SMALL, M
    [J]. DIABETIC MEDICINE, 1990, 7 (01) : 27 - 30