Honda H, Koiwa Y, Takishima T
First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Jpn Circ J. 1994 Jun;58(6):416-25. doi: 10.1253/jcj.58.416.
We previously reported that the application of an external mechanical vibration to the epicardial surface caused a vibration-induced-depression (VID) of left ventricular (LV) function. The magnitude of the VID of peak LV pressure increased as either the amplitude or the frequency of the vibration increased. When LV contractility was altered by the administration of propranolol or by continuous infusion of dobutamine, the magnitude of the VID of peak LV pressure was inversely correlated with LV contractility. These characteristics were observed in open-chest and isolated canine preparations. In the present study, we constructed a muscle model to obtain a theoretical explanation for these effects. This model was first proposed by Gray, Gonda and Cheung, and has been extended in this report to explain twitch tension. This new, improved model is able to explain twitch tension and the effects of external vibration on twitch contraction semi-quantitatively. The successful predictions of the this model support the idea that external vibration directly affects contractile protein and modulates crossbridge kinetics.
我们之前报道过,在心外膜表面施加外部机械振动会导致左心室(LV)功能的振动诱导性降低(VID)。随着振动幅度或频率的增加,左心室峰值压力的VID幅度也会增加。当通过给予普萘洛尔或持续输注多巴酚丁胺改变左心室收缩力时,左心室峰值压力的VID幅度与左心室收缩力呈负相关。这些特征在开胸和离体犬类制备中均有观察到。在本研究中,我们构建了一个肌肉模型以获得对这些效应的理论解释。该模型最初由格雷、贡达和张提出,本报告对其进行了扩展以解释抽搐张力。这个新的改进模型能够半定量地解释抽搐张力以及外部振动对抽搐收缩的影响。该模型的成功预测支持了外部振动直接影响收缩蛋白并调节横桥动力学的观点。