| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1998: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1997: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1996: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Research Abstract |
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.
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