HYPOXIC PRECONDITIONING PRESERVES ANTIOXIDANT RESERVE IN THE WORKING RAT-HEART

被引:93
作者
ENGELMAN, DT
WATANABE, M
ENGELMAN, RM
ROUSOU, JA
KISIN, E
KAGAN, VE
MAULIK, N
DAS, DK
机构
[1] BAYSTATE MED CTR,DEPT SURG,SPRINGFIELD,MA 01107
[2] UNIV PITTSBURGH,DEPT ENVIRONM & OCCUPAT HLTH,PITTSBURGH,PA
关键词
HYPOXIA; HYPOXIC PRECONDITIONING; ANTIOXIDANT RESERVE; ANTIOXIDANTS; ISCHEMIA REPREFUSION INJURY;
D O I
10.1016/S0008-6363(96)88558-0
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective: The aim was to examine whether intracellular antioxidants play a role in myocardial preservation following hypoxic preconditioning. Methods: Isolated working rat hearts were subjected to 30 min ischaemia and 30 min reperfusion. Control hearts were compared to hearts preconditioned with 10 min hypoxia. Left ventricular function and lactate dehydrogenase (LDH) release were measured in each group. Ascorbate dependent (ADAR) and thiol dependent (TDAR) components of the endogenous myocardial antioxidant reserve were assessed using electron spin resonance spectroscopy. Results: Hypoxic preconditioning had no effect on left ventricular function after 10 min reoxygenation. During reperfusion, the hypoxically preconditioned hearts had a significantly increased survival rate, aortic flow, developed pressure, and dP/dt(max), and a reduced lactate dehydrogenase release, compared to non-preconditioned controls (P<0.05). Preconditioned hearts also had significantly higher preservation of baseline ADAR (79%) and TDAR (96%) compared with control hearts, (70%) and (77%), respectively (P<0.05). Conclusions: Hypoxic preconditioning enhances functional recovery and reduces cell necrosis following global ischaemia in the working rat heart. This phenomenon may, in part, be mediated through enhanced ascorbate and thiol components of the antioxidant reserve.
引用
收藏
页码:133 / 140
页数:8
相关论文
共 37 条
  • [1] PRECONDITIONING AGAINST MYOCARDIAL DYSFUNCTION AFTER ISCHEMIA AND REPERFUSION BY AN ALPHA-1-ADRENERGIC MECHANISM
    BANERJEE, A
    LOCKEWINTER, C
    ROGERS, KB
    MITCHELL, MB
    BREW, EC
    CAIRNS, CB
    BENSARD, DD
    HARKEN, AH
    [J]. CIRCULATION RESEARCH, 1993, 73 (04) : 656 - 670
  • [2] EFFECT OF HYPOXIA ON PHOSPHOLIPID-METABOLISM IN PORCINE PULMONARY-ARTERY ENDOTHELIAL-CELLS
    BHAT, GB
    BLOCK, ER
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1992, 262 (05): : L606 - L613
  • [3] ROLE OF MEMBRANE PHOSPHOLIPIDS IN MYOCARDIAL INJURY INDUCED BY ISCHEMIA AND REPERFUSION
    DAS, DK
    ENGELMAN, RM
    ROUSOU, JA
    BREYER, RH
    OTANI, H
    LEMESHOW, S
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1986, 251 (01): : H71 - H79
  • [4] ISCHEMIC PRECONDITIONING AND MYOCARDIAL ADAPTATION TO ISCHEMIA
    DAS, DK
    [J]. CARDIOVASCULAR RESEARCH, 1993, 27 (11) : 2077 - 2079
  • [5] DAS DK, 1989, OXYGEN RADICALS SYST, P97
  • [6] CORRELATION BETWEEN ANTIOXIDANT CHANGES DURING HYPOXIA AND RECOVERY ON REOXYGENATION
    DHALIWAL, H
    KIRSHENBAUM, LA
    RANDHAWA, AK
    SINGAL, PK
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1991, 261 (03): : H632 - H638
  • [7] TISSUE SULFHYDRYL GROUPS
    ELLMAN, GL
    [J]. ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 1959, 82 (01) : 70 - 77
  • [8] FLACK JE, 1991, CIRCULATION, V84, P369
  • [9] FUJI H, 1992, J MOL CELL CARDIO S1, V24, P168
  • [10] BLOCKADE OF ATP-SENSITIVE POTASSIUM CHANNELS PREVENTS MYOCARDIAL PRECONDITIONING IN DOGS
    GROSS, GJ
    AUCHAMPACH, JA
    [J]. CIRCULATION RESEARCH, 1992, 70 (02) : 223 - 233