Honda H, Kinbara K, Tani J, Ogimura T, Koiwa Y, Takagi T, Kikuchi J, Hoshi N, Takishima T
First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Med Eng Phys. 1994 Jan;16(1):47-52. doi: 10.1016/1350-4533(94)90010-8.
In a previous study the authors reported that external mechanical vibration applied to the left ventricular (LV) epicardium induces contractility-dependent depression in LV pressure, stroke volume and stroke work. It was suggested that this depression may be caused by the direct effect of external vibration on contractile protein. In another paper in this issue, it is proved that LV function with various myocardial contractilities and the actual process of deterioration in heart failure are well simulated in the model proposed by Beyar and Sideman, after some modifications have been made. In the study reported here it is assumed that an external mechanical vibration induces sudden reduction in myocardial active stress in the model of Beyar and Sideman; in this way the contractility-dependent effect of external vibration on LV function has been simulated. The results of this simulation support the suggestion that external mechanical vibration directly affects contractile protein and reduces LV function, and it is further suggested that the reduction of LV function induced by external vibration reflects the reserve or tolerance capacity of LV to a sudden reduction of myocardial contractility.
在先前的一项研究中,作者报告称,施加于左心室(LV)心外膜的外部机械振动会导致LV压力、每搏量和每搏功出现与收缩性相关的降低。有人提出,这种降低可能是外部振动对收缩蛋白的直接作用所致。在本期的另一篇论文中,已证明在对Beyar和Sideman提出的模型进行一些修改后,该模型能够很好地模拟具有各种心肌收缩性的LV功能以及心力衰竭恶化的实际过程。在本文所报告的研究中,假设外部机械振动会导致Beyar和Sideman模型中的心肌主动应力突然降低;通过这种方式,模拟了外部振动对LV功能的与收缩性相关的影响。该模拟结果支持了以下观点:外部机械振动直接影响收缩蛋白并降低LV功能,并且进一步表明,外部振动引起的LV功能降低反映了LV对心肌收缩性突然降低的储备或耐受能力。