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在35只切断两侧缓冲神经和迷走神经的麻醉大鼠，观察心室内注射腺苷和心外膜涂布腺苷对延髓腹外侧头端区PGL神经元自发电活动的影响。结果如下：（1）35只大鼠共记录到121个自发放电单位，平均放电频率为22．5±1．9spikes／s。（2）心室内冲击注射腺苷（0．5μmol/kg，0．1ml）时，BP先升（△1．7±0．2kPa，P＜0.001）后降（△4.6土0.5kPa，P＜0．001），HR减慢（△126．5±12.3bpm，P＜0.001）；35个PGL神经元自发放电单位中，30个单位的放电频率由21．9士2．6增至29．2土3．4spikes／s（P＜0．001），3个单位不变，2个单位减少。（3）心外膜涂布腺苷（20mmol/L），动脉血压和心率的变化不明显，22个PGL神经元自发放电频率由18．8土1．9增至26．9土2．8spikes／s（P＜0．001），3个单位的放电频率无变化。（4）静脉注射选择性腺苷A1受体拮抗8－cyclopentyl-1，3－dipropylxanthine（DPCPX，500μg／kg）可完全阻断腺苷对PGL神经元的兴奋效应。（5）在左右房室沟涂布85％酚或切除双侧星状神经节后，腺苷激活PGL神经元的效应即行消失。结果提示，腺苷可通过人受体激活心交感神经传入纤维，进而兴奋PGL神经元。
In 35 anesthetized rats with bilateral buffer nerves and vagus nerves, the effects of intracerebroventricular injection of adenosine and epicardial adenosine on the spontaneous activity of PGL neurons in the rostral ventrolateral medullae were observed. The results are as follows: (1) 35 rats recorded a total of 121 spontaneous discharge units, the average discharge frequency of 22.5 ± 1.9spikes / s. (2) After intraventricular injection of adenosine (0.5μmol / kg, 0.1ml), BP increased first (△ 1.7 ± 0.2kPa, P <0.001) 0.001), and HR decreased (△ 126.5 ± 12.3bpm, P <0.001). The discharge frequency of 30 units in 35 PGL neurons increased from 21.9 ± 2.6 to 29. 2 soil 3.4spikes / s (P <0.001), 3 units unchanged, 2 units decreased. (3) There was no obvious change in arterial blood pressure and heart rate with epicardium adenosine (20mmol / L). The frequency of spontaneous firing of 22 PGL neurons increased from 18.8 ± 1.9 to 26.9 ± 2.8spikes /s(P<0.001) No change in the discharge frequency of 3 units. (4) The selective adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 500μg / kg) can completely block the excitatory effect of adenosine on PGL neurons. (5) The effect of adenosine on activating PGL neurons disappears after coating 85% phenol or removing bilateral stellate ganglion in left and right atrioventricular grooves. The results suggest that adenosine can activate cardiac sympathetic afferent fibers via human receptors, which in turn excite PGL neurons.