摘要
目的和方法：本实验用Ｌ精氨酸和一氧化氮合酶（ＮＯＳ）抑制剂ＬＮＡＭＥ观察内源性一氧化氮（ＮＯ）在高血压性心肌肥厚中的作用。结果：腹主动脉缩窄引起大鼠动脉血压显著升高，左心室重量／体重比值显著增加，左心室ＮＯ含量显著下降；Ｌ精氨酸不影响主动脉缩窄大鼠动脉血压，但减轻左心室重量／体重比值，明显升高左心室ＮＯ含量，加入ＬＮＡＭＥ可消除Ｌ精氨酸的上述作用；主动脉缩窄大鼠给予ＬＮＡＭＥ，动脉血压和左心室／体重比值并没有进一步增加；假手术大鼠给予ＬＮＡＭＥ，血压明显升高，左心室重量／体重比值轻度增加；主动脉缩窄大鼠不论是服用Ｌ精氨酸还是ＬＮＡＭＥ，左心室ｃＧＭＰ含量都明显增加。结论：口服Ｌ精氨酸可减轻主动脉缩窄大鼠心肌肥厚但不影响动脉血压，此作用可能是通过Ｌ精氨酸ＮＯ途径实现的，与ｃＧＭＰ机制无关。
Aim and Methods:
The study investigated the effect of L arginine and nitric oxide synthase (NOS) inhibitor L
NAME on cardiac hypertrophy in coarctation of abdominal aorta (COA) rats and its mechanism.
Results: COA increased arterial pressure and the ratio of left ventricular weight to body weight
(LVW/BW), reduced left ventricular NO content significantly; L Arginine did not affect arterial
pressure, but decreased LVW/BW, increased left ventricular NO content, L NAME abrogated
this effect; In COA rats received L NAME,arterial pressure and LVW/BW did not increased
further, In the sham rats received L NAME, arterial pressure increased significantly, but did
LVW/BW slightly; In COA rats, or in COA rat received L arginine or L NAME, left ventricular
cGMP content increased significantly. conclusion: L Arginine administration decreases cardiac
hypertrophy by NO pathway, which may be independent of cGMP mechanism, but does not
affect hypertension in COA rats.
出处
《中国应用生理学杂志》
CAS
CSCD
1999年第2期100-103,共4页
Chinese Journal of Applied Physiology
基金
广东省自然科学基金
