论文部分内容阅读
目的 :探讨一氧化氮合酶 2 (NOS2 )改善心肌梗死 (MI)后心功能障碍的作用。方法 :选用选择性NOS2抑制剂S 甲基硫脲 (SMT)抑制NOS2。于MI后 4周观察SMT对心功能的影响。结果 :MI组MI后 4周 ,心肌NOS2表达及血浆一氧化氮 (NO)水平均较假手术组升高 [(0 .2 6 1± 0 .0 2 5 )∶(0 .0 92± 0 .0 11)A·μm-2 ,P<0 .0 5 ];(4 6 .6± 4 .2 )∶(30 .6± 2 .1) μmol/L ,P <0 .0 5 ]。SMT干预 4周可使MI后血浆NO水平降低 [(2 6 .6±2 .2 )∶(4 6 .6± 4 .2 ) μmol/L ,P <0 .0 5 ],心室肥厚减轻 ,MI范围缩小 ,心功能改善 [左室舒张末压 (6 .1± 0 .7)∶(11.0± 1.2 )mmHg(1mmHg =0 .133kPa) ,P <0 .0 5 ];中心静脉压 (0 .8± 0 .1)∶(1.6± 0 .2 )mmHg ,P <0 .0 5 ]。结论 :抑制NOS2可以改善MI后心功能。NOS2及其产物NO在MI后心功能障碍的发生发展过程中起促进作用
Objective: To investigate the role of nitric oxide synthase 2 (NOS2) in improving cardiac dysfunction after myocardial infarction (MI). Methods: Selective NOS2 inhibitor methylthiourea (SMT) was used to inhibit NOS2. 4 weeks after MI to observe the impact of SMT on cardiac function. RESULTS: After MI for 4 weeks, the expression of NOS2 and the level of plasma nitric oxide (NO) in MI group were significantly higher than those in sham operation group [(0.261 ± 0.525): (0 .92 ± 0) .0 11) A · μm-2, P <0.05; (46.6 ± 4.2): (30.6 ± 2.1 μmol / L, P <0.05). After intervention with SMT for 4 weeks, plasma NO levels decreased after MI [(26.6 ± 2.2): (46.6 ± 4.2) μmol / L, P <0.05) MI range was reduced and cardiac function was improved [left ventricular end-diastolic pressure (6 .1 ± 0 .7): (11.0 ± 1.2) mmHg (1mmHg = 0.133kPa), P < .8 ± 0 .1): (1.6 ± 0.2 mmHg, P <0.05). Conclusion: Inhibition of NOS2 can improve cardiac function after MI. NOS2 and its NO play an important role in the development of cardiac dysfunction after MI