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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。
Objective To investigate the effects of adenosine on left ventricular myocardial nitric oxide (NO) and nitric oxide synthase (NOS) in rats with ischemic hypertrophy induced by L-thyroxine (L-Thy) The impact of vitality. Methods NO content and NOS activity were measured by benzidine fluorescence spectrophotometry. Results L-Thy-induced hypertrophy of left ventricular myocardial NO content than the normal control group decreased significantly, Ade 5, 10 mg · kg-1 · d-1 ig 3 d, the NO content can be restored to normal levels. Compared with the normal control group, the iNOS activity of left ventricular hypertrophy induced by L-Thy increased significantly; the activity of structural NOS (cNOS) decreased significantly. After Ade 1 0 mg · kg-1 · d-1 ig for 3 days, iNOS activity decreased significantly compared with the pathology group. Ade5, 10 mg · kg-1 · d-1 ig3 d, c NOS activity can be restored to normal levels. CONCLUSION Ade can restore c-NOS activity in left ventricular hypertrophy induced by L-Thy, reduce iNOS activity, increase NO content and exert myocardial protection. Therapeutic effect of Ade on ischemic hypertrophic left ventricle in experimental hyperthyroidism is partially achieved through the NO pathway.