Inhibition of rat ventricular automaticity by adenosine.
Inhibition of rat ventricular automaticity by adenosine.
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腺苷对大鼠心室自律性的抑制。
DOI：
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发表时间：
1985
影响因子：
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通讯作者：
R. Olsson
中科院分区：
文献类型：
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作者：
L. Heller;R. Olsson
本研究旨在描述腺苷对心室起搏器的负性变时作用。用Krebs-Henseleit溶液灌注的离体等容大鼠心室制备物的自发搏动率随着腺苷浓度的增加而降低[log M有效浓度50%（EC 50）= -5.22 +/- 0.17]。普萘洛尔或阿托品对这种腺苷反应的影响的缺乏消除了内源性神经递质的参与。茶碱和8-（4-磺基苯基）茶碱（一种被认为仅作用于细胞表面的类似物）分别将腺苷log M EC 50显著增加至-3.94 +/- 0.22和-3.61 +/- 0.22，这一发现为外部细胞表面受体的参与提供了支持。茶碱引起的自发搏动率的增加，但不是由其类似物，被阻断了普萘洛尔的加入。腺苷类似物R-PIA、S-PIA和NECA的相对变时效力表明细胞表面受体可能是Ri型。腺苷及其类似物的负性变时作用发生在对起搏准备的发展压力没有影响的浓度下。心电图评价表明，在高激动剂浓度，有一个突然改变的电性能的准备，这可以被阻断茶碱及其类似物。
This study was designed to characterize adenosine's negative chronotropic effect on ventricular pacemakers. The spontaneous beating rate of isolated, isovolumic rat ventricular preparations perfused with Krebs-Henseleit solution decreased as the adenosine concentration was increased [log M effective concentration 50% (EC50) = -5.22 +/- 0.17]. The lack of effect of propranolol or atropine on this adenosine response eliminates the involvement of endogenous neurotransmitters. Support for the involvement of an external cell surface receptor was provided by findings that theophylline and 8-(4-sulfophenyl)theophylline, an analogue thought to act solely at the cell surface, significantly increased the adenosine log M EC50 to -3.94 +/- 0.22 and -3.61 +/- 0.22, respectively. An increase in spontaneous beating rate induced by theophylline, but not by its analogue, was blocked by the addition of propranolol. The relative chronotropic potency of the adenosine analogues R-PIA, S-PIA, and NECA suggests that the cell surface receptors may be of the Ri type. The negative chronotropic effects of adenosine and its analogues occurred at concentrations that had no effect on the developed pressure of the paced preparation. Electrocardiographic evaluations indicate that at high agonist concentrations, there was an abrupt alteration in electrical properties of the preparation, which could be blocked by theophylline and its analogue.