Cardioprotective effects of nitroparacetamol and paracetamol in acute phase of myocardial infarction in experimental rats

被引:23
作者
Zhu, YZ [1 ]
Chong, CL
Chuah, SC
Huang, SH
Nai, HS
Tong, HT
Whiteman, M
Moore, PK
机构
[1] Natl Univ Singapore, Dept Pharmacol, Singapore 117597, Singapore
[2] Natl Univ Singapore, Cardiovasc Biol Res Grp, Singapore 117597, Singapore
[3] Fudan Univ, Sch Pharm, Dept Pharmacol, Shanghai, Peoples R China
[4] Natl Univ Singapore Hosp, Emergency Dept, Singapore, Singapore
[5] Natl Univ Singapore, Dept Biochem, Singapore 117548, Singapore
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 2006年 / 290卷 / 02期
关键词
infarct size; cardioprotection;
D O I
10.1152/ajpheart.00572.2005
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
We aimed to determine whether nitroparacetamol (NO-paracetamol) and paracetamol exhibit cardioprotective effects. Myocardial infarction (MI) was induced in rats, and drug treatment was started 1 wk before surgery. Mortality rate and infarct size at 2 days after MI were compared. Treatment groups included vehicle (saline), paracetamol (5 mg-kg(-1)-day(-1)) and NO-paracetamol (15 mg-kg(-1)-day(-1)). Mortality rates for vehicle (n = 80), paracetamol (n = 79), and NO-paracetamol (n = 76) groups were 37.5%, 21.5%, and 26.3%, respectively. Infarct size for the vehicle group was 44.8% (+/- 6.1%) of the left ventricle (LV). For the paracetamol and NO-paracetamol groups, infarct size was 31.3% (+/- 5.6%) and 30.7% (+/- 8.1%) of the LV, respectively. Both paracetamol- and NO-paracetamol-treated groups showed increased activities of catalase and SOD compared with the vehicle group. They could attenuate endothelial, inducible, and neuronal nitric oxide synthase and cyclooxygenase-1 and -2 gene expression after MI. The observation indicates the potential clinical significance of the cardioprotective effects of these drugs.
引用
收藏
页码:H517 / H524
页数:8
相关论文
共 43 条
  • [1] Nitric oxide, platelet function, myocardial infarction and reperfusion therapies
    Alonso, D
    Radomski, MW
    [J]. HEART FAILURE REVIEWS, 2003, 8 (01) : 47 - 54
  • [2] Cytokine-mediated apoptosis in cardiac myocytes - The role of inducible nitric oxide synthase induction and peroxynitrite generation
    Arstall, MA
    Sawyer, DB
    Fukazawa, R
    Kelly, RA
    [J]. CIRCULATION RESEARCH, 1999, 85 (09) : 829 - 840
  • [3] Nitric oxide synthases and cardiac muscle - Autocrine and paracrine influences
    Balligand, JL
    Cannon, PJ
    [J]. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1997, 17 (10) : 1846 - 1858
  • [5] Nitric oxide release and distribution following oral and intraperitoneal administration of nitroaspirin (NCX 4016) in the rat
    Carini, M
    Aldini, G
    Orioli, M
    Piccoli, A
    Rossoni, G
    Facino, RM
    [J]. LIFE SCIENCES, 2004, 74 (26) : 3291 - 3305
  • [6] Molecular basis of cardiotoxicity upon cobra envenomation
    Cher, CDN
    Armugam, A
    Zhu, YZ
    Jeyaseelan, K
    [J]. CELLULAR AND MOLECULAR LIFE SCIENCES, 2005, 62 (01) : 105 - 118
  • [7] EXERCISE-INDUCED MYOCARDIAL CAPILLARY GROWTH IN THE SPONTANEOUSLY HYPERTENSIVE RAT
    CRISMAN, RP
    RITTMAN, B
    TOMANEK, RJ
    [J]. MICROVASCULAR RESEARCH, 1985, 30 (02) : 185 - 194
  • [8] Dai Wangde, 2003, Journal of Cardiovascular Pharmacology and Therapeutics, V8, P277, DOI 10.1177/107424840300800405
  • [9] Endothelial NOS expression and ischemia-reperfusion in isolated working rat heart from hypoxic and hyperoxic conditions
    Felaco, M
    Grilli, A
    Gorbunov, N
    Di Napoli, P
    De Lutiis, MA
    Di Giulio, C
    Taccardi, AA
    Barsotti, A
    Barbacane, RC
    Reale, M
    Conti, P
    [J]. BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS, 2000, 1524 (2-3): : 203 - 211
  • [10] Peroxynitrite is a major contributor to cytokine-induced myocardial contractile failure
    Ferdinandy, P
    Danial, H
    Ambrus, I
    Rothery, RA
    Schulz, R
    [J]. CIRCULATION RESEARCH, 2000, 87 (03) : 241 - 247