Inhibitory effects of excess sympathetic activity on parasympathetic vasodilation in the rat masseter muscle
Inhibitory effects of excess sympathetic activity on parasympathetic vasodilation in the rat masseter muscle
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DOI：
10.1152/ajpregu.00866.2006
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发表时间：
2007-08-01
影响因子：
2.8
通讯作者：
Izumi, Hiroshi
中科院分区：
文献类型：
--
作者：
Ishii, Hisayoshi;Niioka, Takeharu;Izumi, Hiroshi
本研究旨在探讨交感神经紧张性活动对由三叉神经介导的咬肌反射引起的副交感神经血管扩张的影响。切颈上交感干（CST）的同侧增加了咬肌（MBF）的基础血流量水平。使用2毫秒脉冲对CST的外围切割端进行2分钟的电刺激，以依赖的方式降低MBF的强度（0.5-10 V）和频率（0.1-5 Hz）。CST以< 0.5 Hz、5 V、2 ms脉冲刺激2分钟，似乎与支配咬肌脉管系统的CST纤维的自发活动相当，因为这种刺激将MBF的基础水平恢复到预定值。以频率依赖的方式（0.5- 5hz），以5v、2ms脉冲的CST刺激2分钟后，咬肌舌神经中央切端电刺激引起的副交感神经血管舒张明显减弱。静脉注射酚妥拉明可显著降低CST刺激引起的血管收缩，且呈剂量依赖性（0.1-1 mg/kg），但预处理酚妥拉明或心得安均不能影响交感神经对副交感神经血管舒张的抑制。我们的研究结果表明：1)过量的交感神经活动抑制咬肌副交感神经血管舒张；2)α -和β -肾上腺素受体不参与交感神经抑制副交感神经血管舒张，因此一定有其他类型的受体参与了这一反应。
The present study was designed to examine the effect of sympathetic tonic activity on parasympathetic vasodilation evoked by the trigeminal-mediated reflex in the masseter muscle in urethane-anesthetized rats. Sectioning of the superior cervical sympathetic trunk (CST) ipsilaterally increased the basal level of blood flow in the masseter muscle (MBF). Electrical stimulation of the peripheral cut end of the CST for 2 min using 2-ms pulses ipsilaterally decreased in a dependent manner the intensity (0.5-10 V) and frequency (0.1-5 Hz) of the MBF. The CST stimulation for 2 min at < 0.5 Hz with 5 V using 2-ms pulses seems to be comparable with the spontaneous activity in the CST fibers innervating the masseter vasculature, because this stimulation restored the basal level of the MBF to the presectioned values. Parasympathetic vasodilation evoked by electrical stimulation of the central cut end of the lingual nerve in the masseter Muscle was markedly reduced by CST stimulation for 2 min with 5 V using 2-ms pulses in a frequency-dependent manner (0.5-5 Hz). Intravenous administration of phentolamine significantly reduced the vasoconstriction induced by CST stimulation in a dose-dependent manner (0.1-1 mg/kg), but pretreatment with either phentolamine or propranolol failed to affect the sympathetic inhibition of the parasympathetic vasodilation. Our results suggest that 1) excess sympathetic activity inhibits parasympathetic vasodilation in the masseter muscle, and 2) alpha- and beta-adrenoceptors do not contribute to sympathetic inhibition of parasympathetic vasodilation, and thus some other types of receptors must be involved in this response.