Ma X Y, Fan Z Z, He R R, Ho S Y
Department of Physiology, Hebei Medical University, Shijiazhuang.
Sheng Li Xue Bao. 1997 Oct;49(5):504-12.
The effects of intraventricular injection and epicardial application of adenosine on spontaneous electrical activity of nucleus paragigantocellularis lateralis (PGL) neurons in rostral ventrolateral medulla (RVLM) were examined in 35 anesthetized rats with sinoaortic denervation and vagotomy. The results obtained were as follows: (1) The spontaneous discharge of 121 PGL neurons (mean discharge rate: 22.5 +/- 1.9 spikes/s) were recorded in 35 rats. (2) In response to intraventricular injection of adenosine (0.5 mumol/kg), mean arterial pressure (MAP) was initially increased by 1.7 +/- 0.2 kPa(P < 0.001) and subsequently decreased by 4.6 +/- 0.5 kPa(P < 0.001), while the heart rate (HR) was decreased by 126.5 +/- 12.3 bpm (P < 0.001). Of 35 PGL spontaneous discharge units responsive to intraventricular injection of adenosine, 30 showed an average increase from 21.9 +/- 2.6 to 29.2 +/- 3.4 spikes/s (P < 0.001), 3 with no change, while 2 with a decrease. (3) Following epicardial application of 20 mmol/L adenosine, the BP and HR were not significantly changed, while the spontaneous discharge of 22 PGL neurons were increased from 18.8 +/- 1.9 to 26.9 +/- 2.8 spikes/s (P < 0.001), and that of 3 neurons was not changed. (4) The excitatory response of PGL neurons to intraventricular injection or epicardial application of adenosine was completely inhibited by pretreatment with selective adenosine A1-receptor antagonist 8-cyclopentyl-1, 3-dipropylxanthine (DPCPX, 500 micrograms/kg). (5) Following epicardial application of phenol or bilateral stellate ganglionectomy, adenosine failed to affect the activity of PGL neurons. The results obtained indicate that adenosine may stimulate cardiac sympathetic afferents through adenosine A1-receptor, thereby resulting in the activation of PGL neurons.
在35只接受了去窦主动脉神经支配和迷走神经切断术的麻醉大鼠中,研究了脑室内注射和心外膜应用腺苷对延髓头端腹外侧区(RVLM)旁巨细胞外侧核(PGL)神经元自发放电活动的影响。得到的结果如下:(1)在35只大鼠中记录了121个PGL神经元的自发放电(平均放电频率:22.5±1.9次/秒)。(2)脑室内注射腺苷(0.5μmol/kg)后,平均动脉压(MAP)最初升高1.7±0.2kPa(P<0.001),随后降低4.6±0.5kPa(P<0.001),而心率(HR)降低126.5±12.3次/分(P<0.001)。在35个对脑室内注射腺苷有反应的PGL自发放电单位中,30个平均放电频率从21.9±2.6次/秒增加到29.2±3.4次/秒(P<0.001),3个无变化,2个降低。(3)心外膜应用20mmol/L腺苷后,血压和心率无明显变化,而22个PGL神经元的自发放电从18.8±1.9次/秒增加到26.9±2.8次/秒(P<0.001),3个神经元的放电无变化。(4)选择性腺苷A1受体拮抗剂8-环戊基-1,3-二丙基黄嘌呤(DPCPX,500μg/kg)预处理可完全抑制PGL神经元对脑室内注射或心外膜应用腺苷的兴奋反应。(5)心外膜应用苯酚或双侧星状神经节切除术后,腺苷对PGL神经元的活动无影响。得到的结果表明,腺苷可能通过腺苷A1受体刺激心脏交感传入神经,从而导致PGL神经元的激活。