L-NAME诱导大鼠高血压性心脏模型重构的研究  

Hypertension and cardiovascular remodeling induced by the L-NAME in rats.

作　　者：钟南田[1] 符史干[1] 吴卫红[2] 符皎荣[1] 林世珍[1] 

机构地区：[1]海南医学院,海南海口571101 [2]海南医学院附属医院泌尿外科,海南海口571101

出　　处：《中国热带医学》2006年第12期2140-2141,共2页China Tropical Medicine

基　　金：海南省自然科学基金(30018);海南省教育厅高校科研资助项目(Hjkj200112)

摘　　要：目的建立一氧化氮(NO)长期缺乏所致的高血压及心脏重构的动物模型。方法将实验大鼠随机分手术建立腹主动脉缩窄性高血压模型组、L-NAME组和对照组。L-NAME组在对照组的基础上持续用NOS抑制剂L-NAME50mg.kg8[-1].d[-1],8周后测定大鼠平均动脉压(MAP)、心肌的体积密度(VV)、表面积密度(SV)、比表面(S/V)及平均自由程(λ)等各项参数并计算。结果给予L-NAME处理的Sham大鼠,其MAP明显升高,心肌细胞直径增粗,横断面积增大,心肌细胞间的密度增加,组间比较有显著性差异;体视学参数体积密度(Vv)、表面积密度(Sv)显著增大,比表面(S/V)及平均自由程(λ)则变小,组间比较差异有显著性(P<0.05)。结论利用NOS抑制剂L-NAME抑制NO合成,可建立高血压及心脏重构的动物模型。Objective To establish the animal model induced by chronic administration of L- NAME on hypertension and cardiovascular remodeling. Methods Sprague - Dawley rats were divided into three groups： sham - operated group; sham ＋ L - NAME group and coarctation of abdominal aorta group. The mean arterial pressure （ MAP ） were measured in each rat 8 weeks the observation . The stereological parameters such as the myocardial volume density, the myocardial surface density, the myocardial specific s＇arfaee and the mean free path etc. were measured and analyzed. Results The MAP in Sham ＋ L- NAME rats significandy increased, normally increased in the myocardial traverse area and the average diameter, showing significant difference as compared with that of control group in the volume density, the surface density, the specific surface and the mean free path. Conclusion The animal model of hypertension and cardiovascular remodeling can be established by inhibiting the synthesis of NO. 1.

关 键 词：心肌肥大 体视学 NG-硝基左旋精氨酸甲酯 动物模型 

分 类 号：R544.1[医药卫生—心血管疾病]