MECHANISMS FOR ATRIAL ARRHYTHMIAS ASSOCIATED WITH CARDIOMYOPATHY - A STUDY OF FELINE HEARTS WITH PRIMARY MYOCARDIAL-DISEASE
MECHANISMS FOR ATRIAL ARRHYTHMIAS ASSOCIATED WITH CARDIOMYOPATHY - A STUDY OF FELINE HEARTS WITH PRIMARY MYOCARDIAL-DISEASE
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DOI：
10.1161/01.cir.69.5.1036
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发表时间：
1984-01-01
期刊：
影响因子：
37.8
通讯作者：
WIT, AL
中科院分区：
文献类型：
--
作者：
BOYDEN, PA;TILLEY, LP;WIT, AL
本文研究了自发性心肌病猫心脏分离的心律失常和非心律失常心房的细胞电生理和结构特征。根据左心房扩大程度分为3组：轻度(I组)、中度(II组)和重度(III组)。右心房大小相对正常。微电极记录显示，各组大鼠左、右心房均可见不兴奋细胞，但以III组左心房最多。大多数不兴奋的细胞静息膜电位较低。II、III组动物左心房可兴奋细胞静息膜电位、O相最大除极速率、动作电位波幅均显著降低，而右心房可兴奋细胞动作电位正常。乙酰胆碱或去甲肾上腺素通常使原本不产生动作电位的细胞恢复兴奋性。去甲肾上腺素还引起慢反应动作电位和自律性异常，并因延迟后电位而触发活动。病变的心房表现出明显的结构异常，这在第三组猫中最为明显，包括大量的间质纤维化、细胞肥大和变性，以及基底膜增厚。因此，心肌病所致房性快速性心律失常的发生可能与电生理异常和细胞结构改变有关。
The cellular electrophysiologic and structural characteristics of arrhythmic and nonarrhythmic atria isolated from feline hearts with spontaneously occurring cardiomyopathy were studied. The animals were divided into 3 groups according to the degree of left atrial enlargement: mild (group I), moderate (group II) and severe (group III). The right atria were of relatively normal size. Microelectrode recordings showed that inexcitable cells were present in both left and right atria of all groups but were most numerous in the left atria of group III animals. Most inexcitable cells had low resting membrane potentials. There was also a significant reduction in resting membrane potentials, maximum rate of phase O depolarization, and action potential amplitude of excitable cells in left atria of animals in groups II and III, whereas action potentials of excitable cells in the right atria were normal. Acetylcholine or norepinephrine often restored excitability to cells that originally did not generate action potentials. Norepinephrine also caused slow-response action potentials as well as abnormal automaticity and triggered activity due to delayed afterpotentials. The diseased atria showed marked structural abnormalities, which were most pronounced in group III cats, including large amounts of interstitial fibrosis, cellular hypertrophy and degeneration, and thickened basement membranes. Therefore electrophysiologic abnormalities and concurrent changes in cell structure may be involved in the genesis of atrial tachyarrhythmias caused by cardiomyopathy.