Karsanov N V, Sukoian G V, Tatulashvili D R, Karsanov V N, Mamulashvili L D
Biull Eksp Biol Med. 1992 Feb;113(2):146-9.
In vitro on skinned myocardial fibers (SMF) with extracted or functionally inactivated enzymes and membranes of mitochondria, longitudinal sarcoplasmic reticulum, triads and sarcolemma, new evidence of beta-acetyldigoxin and strophanthin K direct stimulating effects on contractile protein system of myocardium has been obtained. It has been revealed in energy release stimulation and force generation, in quantitative (beta-acetyldigoxin) or quantitative and qualitative (strophanthin K) stimulation of energy transduction, in the increase of contractile process cooperativity and Ca-sensitivity of SMF as well as in the SMF relaxation time extension (in the case of strophanthin K). It is suggested that different effects of beta-acetyldigoxin and strophanthin K are due to the differences in the conformations of actomyosin ensembles formed by strong bound (AMESB), which are induced by the influence of these cardiac glycosides. It has been demonstrated that ouabain (strophanthin K) has no direct effect on functioning of AMESB.
在体外对去除或功能失活了线粒体、纵行肌质网、三联体和肌膜的酶及膜的去表皮心肌纤维（SMF）进行研究时，获得了关于β - 乙酰地高辛和毒毛花苷K对心肌收缩蛋白系统直接刺激作用的新证据。这些证据体现在能量释放刺激和力的产生方面，在能量转导的定量（β - 乙酰地高辛）或定量与定性（毒毛花苷K）刺激方面，在收缩过程协同性的增加以及SMF对钙的敏感性方面，还有在SMF松弛时间延长（毒毛花苷K的情况）方面。有人提出，β - 乙酰地高辛和毒毛花苷K的不同作用归因于这些强心苷的影响所诱导形成的强结合肌动球蛋白聚集体（AMESB）构象的差异。已经证明，哇巴因（毒毛花苷K）对AMESB的功能没有直接影响。
