内源性腺苷反应nonreentrant catecholamine-mediated室性心动过速和乙酰胆碱。心肌受体介导作用的证据。
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Lerman BB
内源性腺苷反应nonreentrant catecholamine-mediated室性心动过速和乙酰胆碱。心肌受体介导作用的证据。
循环。1993年2月,87 (2):382 - 90。
- PubMed ID
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8425287 (在PubMed]
- 文摘
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背景:可重入室性心动过速(VT)是不敏感的核苷腺苷。然而,我们曾发现一种nonreentrant, catecholamine-mediated VT和快速的节奏,可以发起了周期长度的依赖,和外源性腺苷敏感以及并发操作。心动过速的机制被认为是由于catecholamine-induced, cAMP-mediated增加细胞内钙,导致延迟afterdepolarizations和触发活动。外源性腺苷的抗心律失常的作用,在医学上这种形式的VT可能是由于受体介导的抑制腺苷酸环化酶或非心血管受体介导的效果,即。,外源性腺苷可以通过改变自主调节VT语气动脉化学感受器激活,在医学和已经被证明可以减少静脉返回,导致减少心脏维度和心肌。澄清这个问题,规避自主和非心血管受体的影响,的反应nonreentrant catecholamine-mediated VT内源性腺苷和乙酰胆碱是评估。方法和结果:第1组(n = 8):双嘧达莫(0.56毫克/公斤增长值),核苷交通阻断剂,增强内源性腺苷的影响,可再生产地废除持续nonreentrant,非自动的,catecholamine-mediated VT的五个病人评估。VT复发与氨茶碱、竞争腺苷A1-receptor拮抗剂。腾喜龙(10毫克注射),胆碱酯酶抑制剂它强化的影响乙酰胆碱的毒蕈碱的胆碱能受体,终止VT在四个四个病人,一个被阿托品逆转的影响。第二组(n = 6):患者可重入VT,双嘧达莫对VT和腾喜龙没有影响周期长度或持续时间。 Group 3 (n = 4): Adenosine and vagal maneuvers had no effect on catecholamine-mediated VT caused by automaticity in three of four patients tested. In one patient, adenosine transiently suppressed VT (< 5 seconds), after which it spontaneously resumed. CONCLUSIONS: The results of this study further delineate the mechanism of a newly recognized form of clinical VT. It can be identified by termination of the tachycardia in response to activation of the adenosine A1 or muscarinic cholinergic receptor, which results in inhibition of adenylate cyclase. These receptor-mediated effects appear to be specific for identifying nonreentrant, nonautomatic, catecholamine-mediated VT.