神经递质对豚鼠左心室流出道自律细胞电活动的影响  

Electrophysiological effects of neurotransmitters on pacemaker cells in guinea pig left ventricular outflow tract

作　　者：赵兰平[1] 张晓云[1] 陈彦静[1] 李建东[1] 张三明[1] 王雪芳[1] 葛赋贵[1] 

机构地区：[1]河北北方学院生理教研室,张家口075000

出　　处：《生理学报》2005年第5期593-598,共6页Acta Physiologica Sinica

基　　金：This work was supported by the Natural Science Foundation of Hebei Province(No.300379).

摘　　要：为研究左心室流出道慢反应自律细胞的神经支配和受体分布,本实验采用标准玻璃微电极细胞内记录技术,分 别观测了肾上腺素能和胆碱能受体激动剂及相应的受体拮抗剂对离体豚鼠左心室流出道组织自发慢反应电位的影响。观测 指标有:最大舒张电位(maximal diastolic potential,MDP)、动作电位幅度(amplitude of action potential,APA)、0相最大去极 速度(maximal rate of depolarization,Vmax)、4相自动去极速度(velocity of diastolic depolarization,VDD)、复极50％时间(50％of duration of action potential,APD50)和90％时间(90％of duration of action potential,APD90)以及自发放电频率(rate of pacemaker firing,RPF)。结果表明:(1)100 μmol／L异丙肾上腺素(isoprenaline,Iso)可使RPF和VDD显著加快(P<0．01),MDP绝对值和 APA显著增大(P<0．05,P<0．01),Vmax加快(P<0．05),APD50缩短(P<0．01),这些变化均可被5 μamol／L心得安拮抗;(2)100 μmol／L肾上腺素(epinephrine,E)可使RPF和VDD加快(P<0．01,P<0．05),APA显著增大(P<0．001),Vmax加快(P<0．05),APD50 和APD90缩短(P<0．05):(3)100μmol／L去甲肾上腺素(norepinephrine,NE)可使VDD和RPF加快(P<0．05),APA显著增大 (P<0．05),Vmax明显加快(P<0．05),APD50缩短(P<0．05),这些变化可被100μmol／L酚妥拉明拮抗;(4)10μmol／L ACh可使 VDD和RPF减慢(P<0．05),APA显著减小(P<0．01),APD50缩短(P<0．05);ACh对APD50的缩短效应可被10 μmol／L阿托 品拮抗(P<0．05)。结果提示:左心室流出道自律细胞膜上可能存在α-肾上腺素能受体(α-adrenergic receptor,α-AR)、β-肾 上腺素能受体(β-adrenergic receptor,β-AR)以及M型胆碱能受体(muscarinic receptor,MR),其自律性电活动可能也接受心交 感神经和心迷走神经调控。This study was designed to explore the innervation of autonomic nervous system and the distribution of receptors on pacemaker cell membrane in guinea pig left ventricular outflow tract （aortic vestibule）. By using conventional intracellular microelectrode technique to record action potentials, autonomic neurotransmitters and antagonists were used to investigate the electrophysiological features and regularities of spontaneous activity of left ventricular outflow tract cells. Electrophysiological parameters examined were： maximal diastolic potential （MDP）, amplitude of action potential （APA）, maximal rate of depolarization （Vmax）, velocity of diastolic depolarization （VDD）, rate of pacemaker firing （RPF）, 50% and 90% of duration of action potential （APD50 and APD90）. The results are listed below： （1） Perfusion with 100 μmol/L isoprenaline （Iso） resulted in a significant increase in Vmax （P〈0.05）, VDD, RPF, and APA （P〈0.01）, a notable decrease in MDP （P〈0.05）, and also a marked shortening in APDso （P〈0.01）. Pretreatment with Iso （100 μmol/L）, propranolol （5 μmol/L） significantly decreased RPF and VDD （P〈0.01）, decreased APA, MDP and Vmax （P〈0.01） notably, prolonged APD50 （P〈0.01） and APD90 （P〈0.05）markedly. （2） Application of 100 μmol/L epinephrine （E） resulted in a significant increase in VDD （P〈0.05）, RPF （P〈0.001）, Vmax （P〈0.05） and APA （P〈0.001）, and a notable shortening in APDso and APD90 （P〈0.05）. （3） Perfusion with 100 μmol/L norepinephrine （NE） led to a significant increase in VDD, RPF, APA and Vmax （P〈0.05）, and a marked shortening in APDso （P〈0.05）. Pretreatment with NE （100 μmol/L）, phentolamine （100 μmol/L） significantly decreased RPF and VDD, MDP and APA （P〈0.01）, decreased Vmax notably （P〈0.05）, prolonged APD50 and APD90 markedly （P〈0.01）.（4） During perfusion with 10 μmol/L acetylcholine （ACh）, VDD and RPF sl

关 键 词：神经递质 豚鼠 心室流出道 电活动 

分 类 号：R33[医药卫生—人体生理学]