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刺激犬的颈迷走神经外周端时可引起心动过缓,而对心脏的抑制作用则逐渐减弱,表现为心率逐渐恢复(但比对照慢)。刺激后DBP立即下降,而SBP系逐渐下降,且下降程度没有DBP大。在刺激时及停止后均出现ES,其分别占刺激次数的47％和53％。在刺激停止后出现PVT(平均加速24.5次/min),PVT期间R波和BP波数不等,SV和BP轻度降低。LVET缩短和PEP/LVET比值升高,出现ES时,SV和BP较ES前显著降低。反映PVT时心脏功能降低。PVT的要理不太清楚,本研究表明反射性迷走撤退在PVT中不起作用。Q-T/Q-S_2比值增大是CA释放的间接证据。心得安可减弱PVT,阿托品可增强PVT,说明PVT由迷走静经释放CA所致。
Stimulation of dog’s vagus nerve at the peripheral end of the dog can cause bradycardia, while the inhibition of the heart is gradually weakened, the performance of the heart rate gradually recovered (but slower than the control). DBP immediately after the decline stimulated, while the SBP Department decreased gradually, and the degree of decline is not DBP. Both ES and ES appeared after stimulation and after stopping, accounting for 47% and 53% of the stimuli respectively. PVT (average acceleration 24.5 beats / min) occurred after stimulation was stopped, and R wave and BP wave number were not equal during PVT, and SV and BP were slightly decreased. LVET shortening and PEP / LVET ratio increased, ES, SV and BP were significantly lower than before ES. Decreased cardiac function reflecting PVT. The rationale for PVT is not clear, and this study shows that reflex vagal withdrawal does not work in PVT. The Q-T / Q-S_2 ratio increase is indirect evidence of CA release. Encore may be weakened PVT, atropine can enhance PVT, indicating that the PVT caused by the vagal release of CA.