Abramochkin D V, Makarenko E Yu, Mitrochin V M, Tian B, Kalugin L Yu, Sutyagin P V, Kamkin A G
Department of Medicine and Biology, N. I. Pirogov Russian State Medical University, Moscow, Russia.
Bull Exp Biol Med. 2012 May;153(1):32-5. doi: 10.1007/s10517-012-1636-5.
In situ microelectrode examination of rat right atrium showed that in physiologically prestretched tissue, NO donor SNAP modifies the repolarization phase of cardiomyocyte AP in a "hump-like" way provoking the development of arrhythmia. Gadolinium both prevents and eliminates this effect attesting to involvement of stretch-activated channels in the development of NO-induced abnormalities. Elevation of SNAP concentration or further stretch of the tissue (presumably, it increases NO concentration) eliminated the hump depolarization induced by moderate SNAP stimulation. Thus, low NO opens the stretch-activated channels while high NO inactivates them.
大鼠右心房的原位微电极检查表明，在生理预拉伸组织中，一氧化氮供体硝普钠（SNAP）以“驼峰样”方式改变心肌细胞动作电位（AP）的复极化阶段，引发心律失常。钆既能预防又能消除这种效应，证明牵张激活通道参与了一氧化氮诱导的异常的发生。增加SNAP浓度或进一步拉伸组织（可能会增加一氧化氮浓度）可消除中度SNAP刺激诱导的驼峰去极化。因此，低浓度一氧化氮会打开牵张激活通道，而高浓度一氧化氮会使其失活。
