【摘要】 目的　探讨诱导型一氧化氮合酶（ｉＮＯＳ） 催化生成的一氧化氮（ＮＯ） 在实验性病毒性心肌炎小鼠心肌损伤中的作用及一氧化氮合酶（ＮＯＳ） 抑制剂Ｎω硝基Ｌ精氨酸甲酯（ＬＮＡＭＥ） 对心肌的保护作用。方法　ＢＡＬＢ／ｃ 鼠２２ 只腹腔感染柯萨奇病毒Ｂ３ 亲心肌细胞株（ＣＶＢ３ｍ）后随机分为两组：ＬＮＡＭＥ组１０ 只（每天给予ＬＮＡＭＥ５ ｍｇ／ｋｇ）及对照组１２ 只。两组小鼠于病毒接种后第８ 天留取血液及心肌标本，分别进行血清ＮＯ含量的间接测定，心肌病理变化半定量分析及心肌ｉＮＯＳ免疫组织化学染色半定量分析。结果　（１） 心肌病变程度：ＬＮＡＭＥ组明显轻于对照组，心肌炎性浸润积分，分别为１．００ ±０．１５ 和２．１７±０．３２（Ｐ＜ ０．０１）；心肌坏死积分，分别为０．７０±０．１５ 和１．８３ ±０．３３（ Ｐ＜ ０．０１） ；（２） 心肌ｉＮＯＳ 免疫组化染色半定量：ＬＮＡＭＥ 组心肌ｉＮＯＳ 染色阳性信号面密度明显低于对照组（０．１０６±０．０１３ 、０．２４４ ±０．０２５ ，Ｐ＜ ０．０１）；（３） 血清ＮＯ 含量：ＬＮＡＭＥ 组明显低于对照组（４．２ ±０．５μｍｏｌ／Ｌ、６．４±０．７ μｍｏｌ／Ｌ， Ｐ＜０．?更多还原

【Abstract】 Objective To investigate the role of nitric oxide (NO) catalyzed by inducible NO synthase (iNOS) in the development of myocardial damage and the protective effect of N ω nitro L arginine methyl ester (L NAME), an inhibitor of NOS on myocardium in experimental murine viral myocarditis Methods Acute viral myocarditis was induced in 22 BALB/c mice by injection of Coxsackievirus B 3m (CVB 3m ) intraperitoneally Ten of the mice were administered L NAME (5 mg/kg/day) Blood and heart samples were obtained from all mice on the 8th day after CVB 3m infection for indirect measurement of serum NO level, histopathological study and iNOS immunohistochemical examination, respectively Results (1) extent of myocardial damage: L NAME treated mice showed a significant reduction in myocarditic lesion compared with that in untreated mice The mean histological scores of inflammatory cell infiltration and myocardial necrosis in the two groups were 1 00±0 15 vs 2 17±0 32 ( P <0 01) and 0 70± 0 15 vs 1 83±0 33 ( P <0 05), respectively (2) myocardial iNOS immunohistochemical hemiquantitative study: The density of positive staining for iNOS in L NAME treated mice was much lower than that in L NAME untreated mice (0 106±0 013 vs 0 244±0 025, P <0 01) (3) serum level of NO: serum level of NO was significantly low in L NAME treated mice compared with that in L NAME untreated mice (4 17±0 47 vs 6 37±0 73 μmol/L, P <0 05) Conclusion Aboundance of iNOS protein was expressed in myocardium Excess amounts of NO catalyzed by iNOS appear to contribute to the progression of myocardial damage. NOS inhibitor L NAME was likely to protect heart from damage in a murine viral myocarditis model更多还原