心室内和心外膜应用腺苷对延髓PGL神经元电活动的影响

EFFECTS 0F INTRAVENTRICULAR AND EPICARDIAL APPLICATION 0F ADENOSINE ON ELECTRICAL ACTIVITY 0F MEDULLARY PGL NEURONS

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。

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 resp0nse to intraventricular injection of adenosine (O.5μmol/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 < O. 001 ), while the heart rate (HR) was decreased by l26-5 t l2-3 bpm (P < 0.001 ). Of 35 PGL spontaneous discharge units responsive to intraventricu1ar 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 2O mmol/L adenosine, the BP and HR were not significantly changed, while the spontaneous discharges 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 Al-receptor antagonist 8-cyclopentyl-1, 3-dipropyhanthine (DPCPX, 500μg/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 Al-receptor, thereby resulting in the activation of PGL neurons.