• 1.吉林大學中日聯(lián)誼醫(yī)院普通外科（長春130031）;;
  • 2.吉林大學第一醫(yī)院中心研究室（長春130021）;;
  • 通訊作者： 宋燕;

目的探討誘導型一氧化氮合酶(iNOS)抑制劑氨基胍對內(nèi)毒素休克大鼠肝臟的組織學和超微結(jié)構(gòu)的影響。方法取雄性Wistar大鼠24只，隨機分為正常對照組、內(nèi)毒素對照組和氨基胍治療組，每組各8只。用大腸桿菌內(nèi)毒素（LPS）復制大鼠內(nèi)毒素性休克模型，氨基胍治療組采用氨基胍治療。觀察并比較三組大鼠肝臟的組織學、超微結(jié)構(gòu)及其血漿一氧化氮（NO）含量的變化。結(jié)果光鏡下可見，內(nèi)毒素組肝組織有散在小膿腫灶形成，肝細胞壞死，中性白細胞浸潤，而氨基胍治療組的肝組織受損程度較輕。電鏡下可見，內(nèi)毒素組的肝細胞核出現(xiàn)融解性空斑，線粒體腫脹和線粒體嵴數(shù)量減少，而氨基胍則對肝臟的結(jié)構(gòu)起到一定的保護作用。內(nèi)毒素對照組血漿NO水平明顯高于正常對照組，給予氨基胍治療后血漿NO水平明顯下降，但仍高于正常對照組。結(jié)論氨基胍通過選擇性抑制iNOS活性，抑制了大鼠內(nèi)毒素休克時過量的NO的產(chǎn)生，保護了肝臟的功能，具有潛在的臨床應(yīng)用價值，值得更深入地研究。

引用本文： 宋文哲,宋燕,譚巖,尹家俊. 氨基胍對內(nèi)毒素休克大鼠肝損傷的保護作用研究. 中國普外基礎(chǔ)與臨床雜志, 2003, 10(4): 347-350. doi: 復制

1. Ruetten H, Southan GJ, Abate A, et al. Attenuation of endotoxininduced multiple organ dysfunction by 1amino2hydroxyguanidine, a potent inhibitor of inducible nitric oxide synthase [Ｊ]. Br J Pharmacol, 1996； 118(2)∶261.
2. Witte K, Schnecko A, Zuther P, et al. Contribution of the nitric oxideguanylyl cyclase system to circadian regulation of blood pressure in normotensive WistarKyoto rats [Ｊ]. Cardiovasc Res, 1995； 30（5）∶682.
3. Yang F, Comtois AS, Fang L, et al. Nitric oxidederived nitrate anion contributes to endotoxic shock and multiple organ injury/dysfunction [Ｊ]. Crit Care Med, 2002； 30(3)∶650.
4. Moncada S, Higgs A. The Largininenitric oxide pathway [Ｊ]. N Eng J Med, 1993； 329(27)∶2002.
5. Thiemermann C .The role of the Larginine： nitric oxide pathway in circulatory shock [Ｊ]. Adv Pharmacol, 1994； 28（1）∶45.
6. Brealey D, Brand M, Hargreaves I, et al. Association between mitochondrial dysfunction and severity and outcome of septic shock [Ｊ]. Lancet, 2002； 360(9328)∶219.
7. Morris SM Jr, Billiar TR. New insights into the regulation of inducible nitric oxide synthesis [Ｊ]. Am J Physiol, 1994； 266（6 Pt 1）∶E829.
8. Billiar TR, Curran RD, Stuehr DJ, et al. An Largininedependent mechanism mediates Kupffer cell inhibition of hepatocyte protein synthesis in vitro [Ｊ]. J Exp Med, 1989； 169(4)∶1467.
9. Nathan C. Nitric oxide as a secretory product of mammalian cells [Ｊ]. FASEB J, 1992； 6(12)∶3051.
  1. 1. Ruetten H, Southan GJ, Abate A, et al. Attenuation of endotoxininduced multiple organ dysfunction by 1amino2hydroxyguanidine, a potent inhibitor of inducible nitric oxide synthase [Ｊ]. Br J Pharmacol, 1996； 118(2)∶261.
  2. 2. Witte K, Schnecko A, Zuther P, et al. Contribution of the nitric oxideguanylyl cyclase system to circadian regulation of blood pressure in normotensive WistarKyoto rats [Ｊ]. Cardiovasc Res, 1995； 30（5）∶682.
  3. 3. Yang F, Comtois AS, Fang L, et al. Nitric oxidederived nitrate anion contributes to endotoxic shock and multiple organ injury/dysfunction [Ｊ]. Crit Care Med, 2002； 30(3)∶650.
  4. 4. Moncada S, Higgs A. The Largininenitric oxide pathway [Ｊ]. N Eng J Med, 1993； 329(27)∶2002.
  5. 5. Thiemermann C .The role of the Larginine： nitric oxide pathway in circulatory shock [Ｊ]. Adv Pharmacol, 1994； 28（1）∶45.
  6. 6. Brealey D, Brand M, Hargreaves I, et al. Association between mitochondrial dysfunction and severity and outcome of septic shock [Ｊ]. Lancet, 2002； 360(9328)∶219.
  7. 7. Morris SM Jr, Billiar TR. New insights into the regulation of inducible nitric oxide synthesis [Ｊ]. Am J Physiol, 1994； 266（6 Pt 1）∶E829.
  8. 8. Billiar TR, Curran RD, Stuehr DJ, et al. An Largininedependent mechanism mediates Kupffer cell inhibition of hepatocyte protein synthesis in vitro [Ｊ]. J Exp Med, 1989； 169(4)∶1467.
  9. 9. Nathan C. Nitric oxide as a secretory product of mammalian cells [Ｊ]. FASEB J, 1992； 6(12)∶3051.