Nakajima Koichi, Furukawa Yasuyuki, Kurogouchi Fumio, Tsuboi Masato, Chiba Shigetoshi
Department of Pharmacology, Shinshu University School of Medicine, Matsumoto, Japan.
J Cardiovasc Electrophysiol. 2002 Sep;13(9):896-901. doi: 10.1046/j.1540-8167.2002.00896.x.
Parasympathetic activity predominates over sympathetic activity not only with respect to heart rate but also with respect to the pacemaker location in the dog heart. After we removed the parasympathetic neural elements in the sinoatrial (SA) fat pad in the right atrium, we observed that cervical vagus stimulation did not decrease the atrial rate, but it did suppress the increase in rate evoked by sympathetic stimulation. We determined whether the pacemaker rate and location were affected by presynaptic or postsynaptic mechanisms.
We determined the earliest activation site by means of isochronic activation mapping of the right atrium of open chest, anesthetized dog hearts. An electrode array, which consisted of 48 unipolar electrodes, was used to record atrial activation. This array covered the three main pacemaker regions, including the SA node region. After parasympathetic nerve fibers in the SA fat pad had been denervated, vagus stimulation at 10 and 30 Hz did not decrease the heart rate, but it attenuated the increase in heart rate evoked by sympathetic stimulation or isoproterenol. Vagus stimulation at 10 Hz during sympathetic stimulation did not shift the earliest activation site from the superior pacemaker region to the SA node region in 11 of 18 experiments. However, vagus stimulation at 10 Hz during isoproterenol infusion shifted the earliest activation site to the SA node region in 11 of 13 experiments. More intense vagus stimulation during combined sympathetic stimulation or isoproterenol infusion shifted the earliest activation site to the SA node or the inferior pacemaker region in 15 of 18 and in all experiments, respectively.
The results suggest that activation of parasympathetic elements not located in the SA fat pad attenuates the increase in heart rate and the shift in pacemaker location evoked by sympathetic activation. The sympathetic and parasympathetic effects interact at presynaptic and postsynaptic sites in the dog heart.
副交感神经活动不仅在心率方面，而且在犬心脏起搏点位置方面均占主导地位。在我们去除右心房窦房（SA）脂肪垫中的副交感神经成分后，我们观察到颈迷走神经刺激并未降低心房率，但它确实抑制了交感神经刺激引起的心率增加。我们确定了起搏心率和位置是否受突触前或突触后机制的影响。
我们通过对开胸、麻醉的犬心脏右心房进行等时激活标测来确定最早的激活部位。使用由48个单极电极组成的电极阵列记录心房激活。该阵列覆盖了三个主要起搏区域，包括窦房结区域。在SA脂肪垫中的副交感神经纤维去神经支配后，10Hz和30Hz的迷走神经刺激并未降低心率，但减弱了交感神经刺激或异丙肾上腺素引起的心率增加。在18个实验中的11个实验中，交感神经刺激期间10Hz的迷走神经刺激并未将最早的激活部位从上部起搏区域转移至窦房结区域。然而，在13个实验中的11个实验中，异丙肾上腺素输注期间10Hz的迷走神经刺激将最早的激活部位转移至窦房结区域。在联合交感神经刺激或异丙肾上腺素输注期间，更强的迷走神经刺激分别在18个实验中的15个实验和所有实验中将最早的激活部位转移至窦房结或下部起搏区域。
结果表明，位于SA脂肪垫之外的副交感神经成分的激活减弱了交感神经激活引起的心率增加和起搏点位置的转移。交感神经和副交感神经效应在犬心脏的突触前和突触后部位相互作用。
