Li Y L, He R R
Department of Physiology, Hebei Medical College, Shijiazhuang, China.
Zhongguo Yao Li Xue Bao. 1995 Jan;16(1):42-6.
To investigate the electrophysiological effects of adenosine deaminase (ADase, an enzyme converting adenosine to inosine and ammonia), 8-phenyltheophylline (8-PT, a nonselective antagonist of adenosine receptors) and glibenclamide (Gli, a potent blocker of ATP-sensitive K+ channels) on anoxic pacemaker cells of SA node.
Anoxia of pacemaker cells in SA node of guinea-pig was induced by perfused for 20 min with a modified K-H solution gassed with 100% N2 deprived of glucose. Parameters of action potentials including maximal diastolic potential (MDP), amplitude of action potential (APA), duration of 90% repolarization (APD90), maximal rate of depolarization (Vmax), rate of pacemaker firing (RPF), and velocity of diastolic (phase 4) depolarization (VDD) were recorded using intracellular microelectrodes.
Anoxia increased MDP, APA, and Vmax and decreased VDD, RPF in a time-dependent manner. ADase 10 U.L-1, 8-PT 0.1 mumol.L-1 and Gli 10 mumol.L-1 significantly attenuated the electrophysiological changes of pacemaker cells in sincatrial node induced by anoxia.
Endogenous adenosine and ATP-sensitive K+ channels may play an important role in the generation of anoxic bradycardia in guinea pigs.
研究腺苷脱氨酶（ADase，一种将腺苷转化为肌苷和氨的酶）、8-苯基茶碱（8-PT，一种腺苷受体非选择性拮抗剂）和格列本脲（Gli，一种ATP敏感性钾通道强效阻滞剂）对窦房结缺氧起搏细胞的电生理作用。
用不含葡萄糖且用100%氮气充气的改良K-H溶液灌注豚鼠窦房结起搏细胞20分钟，诱导缺氧。使用细胞内微电极记录动作电位参数，包括最大舒张电位（MDP）、动作电位幅度（APA）、90%复极化持续时间（APD90）、最大去极化速率（Vmax）、起搏发放频率（RPF）和舒张期（4期）去极化速度（VDD）。
缺氧以时间依赖性方式增加MDP、APA和Vmax，并降低VDD、RPF。10 U·L-1的ADase、0.1 μmol·L-1的8-PT和10 μmol·L-1的Gli显著减弱了缺氧诱导的窦房结起搏细胞的电生理变化。
内源性腺苷和ATP敏感性钾通道可能在豚鼠缺氧性心动过缓的发生中起重要作用。
