Miyamoto Tadayoshi, Kawada Toru, Yanagiya Yusuke, Inagaki Masashi, Takaki Hiroshi, Sugimachi Masaru, Sunagawa Kenji
Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Osaka 565-8565, Japan.
Am J Physiol Heart Circ Physiol. 2004 Aug;287(2):H860-5. doi: 10.1152/ajpheart.00752.2003. Epub 2004 Mar 11.
Complex sympathovagal interactions govern heart rate (HR). Activation of the postjunctional beta-adrenergic receptors on the sinus nodal cells augments the HR response to vagal stimulation, whereas exogenous activation of the presynaptic alpha-adrenergic receptors on the vagal nerve terminals attenuates vagal control of HR. Whether the alpha-adrenergic mechanism associated with cardiac postganglionic sympathetic nerve activation plays a significant role in modulation of the dynamic vagal control of HR remains unknown. The right vagal nerve was stimulated in seven anesthetized rabbits that had undergone sinoaortic denervation and vagotomy according to a binary white-noise signal (0-10 Hz) for 10 min; subsequently, the transfer function from vagal stimulation to HR was estimated. The effects of beta-adrenergic blockade with propranolol (1 mg/kg i.v.) and the combined effects of beta-adrenergic blockade and tonic cardiac sympathetic nerve stimulation at 5 Hz were examined. The transfer function from vagal stimulation to HR approximated a first-order, low-pass filter with pure delay. beta-Adrenergic blockade decreased the dynamic gain from 6.0 +/- 0.4 to 3.7 +/- 0.6 beats x min(-1) x Hz(-1) (P < 0.01) with no alteration of the corner frequency or pure delay. Under beta-adrenergic blockade conditions, tonic sympathetic stimulation did not further change the dynamic gain (3.8 +/- 0.5 beats x min(-1) x Hz(-1)). In conclusion, cardiac postganglionic sympathetic nerve stimulation did not affect the dynamic HR response to vagal stimulation via the alpha-adrenergic mechanism.
复杂的交感迷走神经相互作用调节心率(HR)。窦房结细胞上节后β-肾上腺素能受体的激活增强了心率对迷走神经刺激的反应,而迷走神经末梢上突触前α-肾上腺素能受体的外源性激活则减弱了迷走神经对心率的控制。与心脏节后交感神经激活相关的α-肾上腺素能机制在心率动态迷走神经控制的调节中是否起重要作用尚不清楚。对7只经窦主动脉去神经和迷走神经切断术的麻醉兔,根据二元白噪声信号(0 - 10 Hz)刺激右侧迷走神经10分钟;随后,估计从迷走神经刺激到心率的传递函数。研究了普萘洛尔(1 mg/kg静脉注射)的β-肾上腺素能阻断作用以及β-肾上腺素能阻断与5 Hz持续性心脏交感神经刺激的联合作用。从迷走神经刺激到心率的传递函数近似于一个具有纯延迟的一阶低通滤波器。β-肾上腺素能阻断使动态增益从6.0±0.4降至3.7±0.6次搏动×分钟-1×赫兹-1(P < 0.01),而转折频率或纯延迟无改变。在β-肾上腺素能阻断条件下,持续性交感神经刺激未进一步改变动态增益(3.8±0.5次搏动×分钟-1×赫兹-1)。总之,心脏节后交感神经刺激并未通过α-肾上腺素能机制影响心率对迷走神经刺激的动态反应。