Electrical responses of guinea pig coronary artery to transmural stimulation.
Electrical responses of guinea pig coronary artery to transmural stimulation.
复制标题
豚鼠冠状动脉对透壁刺激的电反应。
DOI：
10.1161/01.res.62.3.585
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发表时间：
1988
影响因子：
20.1
通讯作者：
Kreulen,DL
中科院分区：
文献类型：
--
作者：
Keef,KD;Kreulen,DL
豚鼠回旋冠状动脉的孤立节段在细胞内记录的同时用短持续时间（0.05毫秒）脉冲进行透壁刺激。静息膜电位为-60.3 +/- 4.3 mV (n = 66)。用单次刺激引起瞬时去极化（TD），其幅度随刺激强度分级。 47 +/- 5 mV 的动作电位叠加在高于 -48 +/- 4 mV 阈值膜电位的 TD 上。尖峰之后，观察到需要 77 +/- 33 秒的缓慢复极化期。重复刺激导致 TD 求和和缓慢去极化（小于或等于 21 mV），持续长达 90 秒。当膜随着 [K]o 增加而去极化时，TD 幅度减小；而当膜通过向缺钾组织添加钾而超极化时，TD 幅度增强。酚妥拉明 (10(-5) M)、哌唑嗪 (10(-6) M)、胍乙啶 (2 X 10(-5) M)、α,β-亚甲基 ATP (2 X 10(-5) M)、河豚毒素 (10(-6) M) 和 10-20 mM 去甲肾上腺素不会阻断 TD、动作电位或减慢去极化。冷藏（4 摄氏度）4 天后 TD 被消除，并且在含有 0.25 mM CaCl2 的 2.25 mM CdCl2 溶液中显着降低。乙酰胆碱（10（-8）M至10（-5）M）产生膜超极化并降低TD的幅度并改变其时程。阿托品（10（-5）M）阻断乙酰胆碱的作用，但对神经刺激的反应没有影响。这些观察结果表明，TD 表现出通过释放其他血管中的神经递质物质而获得的兴奋性连接电位的一些但不是全部特性。如果这些 TD 是神经事件，那么它们一定涉及除去甲肾上腺素、乙酰胆碱或 ATP 之外的递质。
Isolated segments of the guinea pig circumflex coronary artery were stimulated transmurally with brief duration (0.05 msec) pulses while recording intracellularly. Resting membrane potential was -60.3 +/- 4.3 mV (n = 66). Transient depolarizations (TDs) graded in amplitude with stimulus intensity were elicited with single stimuli. An action potential of 47 +/- 5 mV was superimposed upon the TD above a threshold membrane potential of -48 +/- 4 mV. Following the spike, a period of slow repolarization requiring 77 +/- 33 seconds was observed. Repetitive stimulation led to summation of TDs and a slow depolarization (less than or equal to 21 mV) that persisted for up to 90 seconds. The TD was reduced in amplitude when the membrane was depolarized with increased [K]o and enhanced when the membrane was hyperpolarized by adding potassium back to a potassium-depleted tissue. Phentolamine (10(-5) M), prazosin (10(-6) M), guanethidine (2 X 10(-5) M), alpha,beta-methylene ATP (2 X 10(-5) M), tetrodotoxin (10(-6) M), and 10-20 mM norepinephrine did not block TDs, action potentials, or slow depolarization. TDs were abolished following cold storage (4 degrees C) for 4 days and significantly reduced in a 2.25-mM CdCl2 solution with 0.25 mM CaCl2. Acetylcholine (10(-8) M to 10(-5) M) produced membrane hyperpolarization and reduced the amplitude of TDs and altered their time course. Atropine (10(-5) M) blocked the effects of acetylcholine but had no effect on the response to nerve stimulation. These observations indicate that TDs exhibit some, but not all, of the properties characteristic of excitatory junction potentials obtained with release of neurotransmitter substances in other vessels. If these TDs are neural events, they must involve a transmitter other than norepinephrine, acetylcholine, or ATP.