Modulation of carcliac function by L-Arginine NO system

L-精氨酸NO系统对胰功能的调节

• 批准号: 08670751
• 负责人: IKEDA Jun
• 金额: $ 1.54万
• 依托单位: Tohoku University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1996
• 资助国家: 日本
• 起止时间: 1996 至 1998
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-08670751/
• 关键词: Sympathetic Nervous System; LV function; L-Arginine NO System; NOS inhibiter; NO合成酵素阻害剤

In this project, we examined to clarify whether the inhibition of L-arginine NO system augments the positive inotropic response on the left ventricle to direct stimulation of the sympathetic nervous system in vivo.We performed electrical stimulation on left stellate ganglion (LSG) for 1min in submaximal (5V-2.5, 5 and 10Hz) and supramaximal intensities(10V-l0Hz) to twelve anesthetized and vagotomized dogs. Next, in the same dogs, Nw-nitro L-arginine methylester (L-NAME) at 0.1mg was infused into the left anterior descending (LAD) coronary artery, and the LSG stimulation was repeated in the same protocol. Finally, L-arginine at 100mg was infused into the LAD artery, and the same LSG stimulation was repeated. We applied the maximum of the first derivative of left ventricular pressure (LVmax dP/dt) as the index of the myocardial contraction. We measured the plasma epinephrine and norepinephrine concentrations in the coronary sinus (Ecs, NEcs) at 5V-2.5Hz before and after L-NAME treatment in five of twelve dogs.L-NAME treatment significantly augmented the inotropic response on left ventricle (percent change in the LVmax dP/dt) to the LSG submaximal stimulation trains from 164*13 to.212*21 (p<0.03), from 187*15 to 234*25 (p<0.05) and from 220*19 to 28033% (p<0.05), respectively. This response reversed by L-arginine treatment. However, the inotropic response to the supramaximal stimulation train did not change after L-NAME and L-arginine treatment. L-NAME significantly increased NEcs from 0.69*0.41 to 1.00*0.52ng/ml while this did not change Ecs.

在这个项目中，我们检查了L-精氨酸NO系统的抑制是否会增强左心室的正性肌力反应，以直接刺激体内的交感神经系统。我们以次最大强度（5V-2.5、5和10Hz）和超最大强度（10V-10Hz）对左星状神经节（LSG）进行1分钟的电刺激，以 十二只被麻醉和迷走神经切断的狗。接下来，在相同的狗中，将0.1mg Nw-硝基L-精氨酸甲酯（L-NAME）注入左冠状动脉前降支（LAD），并以相同的方案重复LSG刺激。最后，将100mg L-精氨酸注入LAD动脉，并重复相同的LSG刺激。我们采用左心室压力一阶导数的最大值（LVmax dP/dt）作为心肌收缩的指标。我们测量了 12 只狗中的 5 只在 L-NAME 治疗前后在 5V-2.5Hz 下冠状窦 (Ecs、NEcs) 的血浆肾上腺素和去甲肾上腺素浓度。L-NAME 治疗显着增强了左心室对 164*13 LSG 次最大刺激序列的正性肌力反应（LVmax dP/dt 的百分比变化） 分别从 187*15 到 234*25 (p<0.05) 到 212*21 (p<0.03)、从 220*19 到 28033% (p<0.05)。 L-精氨酸治疗可逆转这种反应。然而，L-NAME 和 L-精氨酸治疗后，对超最大刺激序列的正性肌力反应没有改变。 L-NAME 显着地将 NEcs 从 0.69*0.41 增加到 1.00*0.52ng/ml，但这并没有改变 Ecs。

项目成果

T.Takita, J.Ikeda, et al.: "Nitric Oxide Modulates Sympatictic Control on Left ventriclar Contraction in vive" Journal of the Autonomic IVrvons System. (in press). (1998)

T.Takita、J.Ikeda 等人：“一氧化氮在体内调节左心室收缩的症状控制”自主 IVrvons 系统杂志。