Saman S, Coetzee W A, Opie L H
Ischaemic Heart Disease Research Unit, University of Capetown, Medical School, Observatory, South Africa.
J Mol Cell Cardiol. 1988 Feb;20(2):91-5. doi: 10.1016/s0022-2828(88)80022-1.
Controversy exists about the role of an increased level of tissue cyclic adenosine 3'-5' monophosphate (cAMP) in the genesis of early ischemic ventricular arrhythmias. Evidence for an arrhythmogenic role for cAMP was proposed by Podzuweit et al. (1978) and Opie et al. (1979) who argued that ischemic ventricular fibrillation was associated with increased levels of tissue cAMP in the ischemic zone. Lubbe et al. (1978) found that infusion of dibutyryl (dBcAMP), or the beta-adrenergic stimulant epinephrine, or the phosphodiesterase inhibitor theophylline, all produced a marked fall in the ventricular fibrillation threshold and an increase in the duration of the vulnerable period of the isolated perfused rat heart. In contrast, Muller et al. (1986) recently showed that prevention of ventricular fibrillation by beta-adrenergic blockade is not directly associated with decreased levels of cAMP, while Manning et al. (1985) used forskolin to stimulate adenylate cyclase and found that the markedly elevated tissue cAMP levels in the rat heart did not promote ischemic or reperfusion arrhythmias. Some of these contradictions could be resolved if the electrophysiological mechanisms by which increased levels of cAMP might predispose to arrhythmias were better understood. It is known that intracellular injection of cAMP into cardiac myocytes can enhance delayed afterdepolarizations (DADs; Matsuda et al. 1982) and that DADs may explain certain arrhythmias such as those evoked by digitalis toxicity (Ferrier, 1977) or reperfusion (Ferrier et al. 1985).(ABSTRACT TRUNCATED AT 250 WORDS)
组织中环磷酸腺苷（cAMP）水平升高在早期缺血性室性心律失常发生过程中的作用存在争议。Podzuweit等人（1978年）和Opie等人（1979年）提出了cAMP具有致心律失常作用的证据，他们认为缺血性心室颤动与缺血区组织cAMP水平升高有关。Lubbe等人（1978年）发现，输注二丁酰cAMP（dBcAMP）、β-肾上腺素能兴奋剂肾上腺素或磷酸二酯酶抑制剂茶碱，都会使离体灌注大鼠心脏的心室颤动阈值显著降低，易损期持续时间增加。相比之下，Muller等人（1986年）最近表明，β-肾上腺素能阻滞剂预防心室颤动与cAMP水平降低并无直接关联，而Manning等人（1985年）使用福斯可林刺激腺苷酸环化酶，发现大鼠心脏中组织cAMP水平显著升高并未促进缺血性或再灌注性心律失常。如果能更好地理解cAMP水平升高可能导致心律失常的电生理机制，其中一些矛盾或许就能得到解决。已知向心肌细胞内注射cAMP可增强延迟后去极化（DADs；Matsuda等人，1982年），且DADs可能解释某些心律失常，如洋地黄毒性（Ferrier，1977年）或再灌注（Ferrier等人，1985年）所诱发的心律失常。（摘要截选至250词）
