Mechanism of atropine-resistant atrioventricular block during inferior myocardial infarction: possible role of adenosine.

Mechanism of atropine-resistant atrioventricular block during inferior myocardial infarction: possible role of adenosine.
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下壁心肌梗死时阿托品抵抗性房室传导阻滞的机制:腺苷的可能作用。

DOI:
10.1016/s0735-1097(86)80406-5
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发表时间:
1986
影响因子:
24
通讯作者:
Belardinelli,L
Belardinelli,L
中科院分区:
医学1区
文献类型:
--
作者:
WesleyJr,RC;Lerman,BB;DiMarco,JP;Berne,RM;Belardinelli,L

文献摘要

被引文献

相似文献

急性下壁心肌梗死时房室传导阻滞的机制尚不完全清楚。副交感神经张力增加是通常假设的因素;然而,经常观察到阿托品给药后持续性房室传导阻滞。腺苷是一种内源性缺血代谢产物,对房室结传导有明显的抑制作用。在本报告中,一位急性下壁心肌梗塞的病人,其阿托品抵抗性房室传导阻滞的发作被竞争性腺苷拮抗剂氨茶碱逆转。这一观察结果表明腺苷在缺血诱导的房室结阻滞的介导中的作用。
Mechanisms responsible for atrioventricular (AV) block during acute inferior myocardial infarction are only partially understood. Increased parasympathetic tone is the factor usually postulated; however, persistence of AV block after atropine administration is frequently observed. Adenosine, an endogenous ischemic metabolite, has well established depressant effects on AV node con- auction. In this report, an episode of atropine-resistant AV block was reversed by aminophylline, a competitive adenosine antagonist, in a patient with an acute inferior myocardial infarction. This observation suggests a role for adenosine in the mediation of ischemia-induced AV node block.