摘要
目的 了解一氧化氮 (NO)对未成熟心肌缺血 /再灌注损伤的保护作用。方法 2 4只 3～ 4周龄幼兔 ,随机分为 4组 ,每组 6只 :Ⅰ组 ,正常对照组 ;Ⅱ组 ,缺血 /再灌注损伤组 ;Ⅲ组 ,L -精氨酸 (3 0 0mg/kg)组 ;Ⅳ组 ,L -硝基精氨酸甲酯 (L -NAME ,10mg/kg)组。建立活体心脏缺血 /再灌注损伤模型 ,监测左心室血流动力学变化及观察心肌超微结构变化。结果 给药后缺血前 ,与Ⅰ组相比 ,Ⅲ组LVDP及±dp/dtmax下降 ,Ⅳ组LVDP及±dp/dtmax则升高 (P <0 .0 5) ;再灌注 60min ,Ⅱ组和Ⅳ组的LVDP及±dp/dtmax低于Ⅲ组 (P <0 .0 1)。电镜观察显示 ,Ⅱ组和Ⅳ组心肌细胞水肿、线粒体损伤明显 ,而Ⅲ组的细胞及线粒体损伤较轻。结论 一氧化氮能减轻未成熟心肌的缺血 /再灌注损伤 。
Objective To study the protective effect of nitrogen monoxide on the immature myocardium in the in-vivo rabbit immature heart model undergoing ischemia and reperfusion.?Me thod Twenty-four young rabbits (aged 3 to 4 weeks) were randomly div ided into 4 groups ( n =6 each): group Ⅰ, normal control; group Ⅱ, ischemia /reperfusion injury; group Ⅲ, NO-donor (L-arginine 300 mg/kg) group; group Ⅳ, NOS inhibitor (L-NAME 10 ng/kg) group.?Results Before my ocardial ischemia, the LVDP and ±dp/dt max were lower in group Ⅲ than in group Ⅰ, but were higher in group Ⅳ than in group Ⅰ ( P <0.05). One hour a fter reperfusion, the LVDP and ±dp/dt max were higher in group Ⅲ than in groups Ⅱ and Ⅳ ( P <0.01). Significant myocardial ultrastructural changes were found in groups Ⅱ and Ⅳ, with edema and severe damages in myocardium and in mitochondria, but the structural changes were much less serious in group Ⅲ. ?Conclusion The protection of immature myocardium agains t ischemia/reperfusion injury by NO maybe relates to its influence on the energy metabolism of mitochondria.
出处
《徐州医学院学报》
CAS
2003年第6期474-477,共4页
Acta Academiae Medicinae Xuzhou
基金
江苏省麻醉学重点实验室开放课题 (K9843 )
