摘要
目的 研究腺苷 (Adenosine,Ade)对 L-甲状腺素 (L-thyroxine,L-Thy)诱发的大鼠缺血性肥厚左室心肌中一氧化氮 (NO)含量和一氧化氮合酶 (NOS)活力的影响。方法 NO含量和 NOS活力采用联苯胺荧光分光光度法测定。结果 L-Thy诱发的肥厚左室心肌中的 NO含量比正常对照组显著下降 ,Ade 5 ,1 0 mg· kg- 1·d- 1 ig3 d后 ,可使 NO含量恢复到正常水平。与正常对照组相比 ,L-Thy诱发的肥厚左室心肌中诱导型 NOS(i NOS)活力显著升高 ;结构型 NOS(c NOS)活力显著下降。 Ade 1 0 mg· kg- 1 · d- 1 ig 3 d后 ,i NOS活力比病理组显著下降。Ade5 ,1 0 mg·kg- 1·d- 1 ig3 d后 ,c NOS活力均可恢复至正常水平。结论 Ade通过恢复 L-Thy诱发的大鼠肥厚左室心肌中的 c NOS活力 ,降低 i NOS活力 ,升高 NO含量 ,发挥心肌保护作用。Ade对实验性甲亢大鼠缺血性肥厚左室的治疗作用部分是通过 NO通路实现的。
AIM Effects of adenosine (Ade) on left ventricular NO content and NOS activity in rat hypertrophic heart induced by L thyroxine ( L Thy) were studied. METHODS The cardiac hypertrophy was induced by ig L Thy 4 mg·kg -1 ·d -1 and treated with Ade. NO content and NOS activity were measured by benzidine fluorescence spectrophotometry. RESULTS\ Compared with that of the control group, the left ventricular NO contents of hypertrophy group were significantly decreased. After treating with ig Ade 5 or 10 mg·kg -1 ·d -1 for 3 days, the NO contents were recovered to normal state. Compared with that of the control group, the left ventricular iNOS activity of hypertrophy group was significantly increased. Meanwhile, the left ventricular cNOS activity was significantly decreased. After treating with ig Ade 10 mg·kg -1 ·d -1 for 3 days, the iNOS activity was reduced significantly. After treating with ig Ade 5 or 10 mg·kg -1 ·d -1 for 3 days, the cNOS activity was recovered and significantly increased. CONCLUSION\ Ade could recover the cNOS activity and inhibit the iNOS activity in left ventricular of hypertrophic heart induced by L Thy and then modulate the NO content. The therapeutic effect of Ade on cardiac hypertrophy was mediated, in part, through the NO pathway.
出处
《中国药科大学学报》
CAS
CSCD
北大核心
2002年第4期335-338,共4页
Journal of China Pharmaceutical University