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EFFECTS OF MYOCARDIAL ISCHEMIA REPERFUSION INJURY ON L-ARGININE/NITRIC OXIDE SYSTEM IN RAT HEART
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- Author:
- No author available
- Journal Title:
- ACTA PHYSIOLOGICA SINICA
- Issue:
- 1
- DOI:
- 10.3321/j.issn:0371-0874.1999.01.005
- Key Word:
- 心肌;缺血-再灌注损伤;一氧化氮;L-精氨酸转运;大鼠
Abstract： 为探讨大鼠心脏缺血-再灌注损伤(IRI)期间一氧化氮(NO)生成增加的环节和过程.本实验用离体灌流大鼠心脏,预灌流15 min,停灌45 min,取30 ml KH 液循环灌流15 min,观察冠脉流出液中细胞胞浆酶(LDH)、蛋白质、肌红蛋白漏出量和NO-2含量、心肌组织NOS活性、L-精氨酸(L-Arg)转运的改变.结果显示,心脏IRI后,冠脉流出液中LDH活性、蛋白质和肌红蛋白量较对照组分别增加4.1,5.4和1倍(均P<0.01).NO-2含量增加1.2倍(P<0.01).心肌组织tNOS活性、iNOS活性和cNOS活性分别增加48.2%、43.2%和52.1%(均P<0.01).NO-2含量与心肌组织iNOS活性呈正相关,(r=0.7942,P<0.01).心肌组织L-Arg转运呈现高、低亲和两种方式.IRI组心肌L-Arg转运能力增强,最大转运速率(Vmax)较对照组升高48%(低亲和,P<0.05)和2倍(高亲和,P<0.01); 低亲和Km值降低47.4%(P<0.05),高亲和Km值改变无统计学意义.L-Arg转运高、低亲和转运载体的Vmax与iNOS活性、NO-2含量均呈高度正相关关系.结果提示: 心脏IRI时,心肌L-Arg转运能力增强,主要通过激活iNOS而增加NO的生成,L-Arg转运是NO生成的重要环节.
- [1]J W, Kim,E I, Closs,L M, Albritton,etc.Transport of cationic amino acids by the mouse ecotropic retrovirus receptor.[J].1991,352(6337).
- [2]Y, Nonami.The role of nitric oxide in cardiac ischemia-reperfusion injury.[J].1997,61.
- [3]X.-S. LI,Y. URIUDA,Q.-D. WANG,etc.Role ofl-arginine in preventing myocardial and endothelial injury following ischaemia/reperfusion in the rat isolated heart[J].1996,156(1).
- [4]W, Durante,L, Liao,I, Iftikhar,etc.Differential regulation of L-arginine transport and nitric oxide production by vascular smooth muscle and endothelium.[J].1996,78.
- [5]张新波,黄海鹭,张灵芝,等.一氧化氮合成酶（NOS）活性的测定及其应用[J].1994,(0S1).
- [6]Kukreja RC,Jesse RL,Hess ML,etc.Sustained inhibition of nitric oxide by NG-nitro-L-arginine improves myocardial function following ischemia/reperfusion in isolated perfused rat heart.[J].1995,27(1).
- [7]R G, Bogle,A R, Baydoun,J D, Pearson,etc.L-arginine transport is increased in macrophages generating nitric oxide.[J].1992,284 ( Pt 1).
- [8]K. Node,M. Kitakaze,H. Kosaka,etc.Plasma Nitric Oxide End Products Are Increased in the Ischemic Canine Heart[J].1995,211(2).