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关于瓣膜平面的机制(作者译)

[On the mechanism of valve plane (author's transl)].

作者信息

Lunkenheimer P P, Adami H, Trost U, Wohlfeil H, Stürje H, Ising A

出版信息

Thoraxchir Vask Chir. 1975 Apr;23(2):131-7. doi: 10.1055/s-0028-1096935.

Abstract

A detailed description of the functional sequence and mechanism of the valve plane movements is given as an extension of the studies on the functional morphology of cardiac movements. The valve plane mechanism is driven in the small, rapidly beating heart by the contraction of the external and internal spiral fibres of the myocardium which decreases the width of the chamber. The atrium is enlarged during systole by the descent of the valvular ring towards the apex. The auricular apendices must act as a compensation reservoir giving the atrial wall the necessary freedom of movement within the pericardial dome. Under these working conditions (hypovolaemia, decreased venous return pathophysiological consequences are discernible as subendocardial bleeding secondary to increased sliding movement of the inner layer of the myocardium against the middle layer. Chamber dilation as a consequence of endocardial fibrosis is explained as a result of progressive rigidity of endo-epicardial fixation. These structural changes progressively impair the systolic-diastolic changes in wall thickness.

摘要

作为对心脏运动功能形态学研究的扩展,本文给出了瓣膜平面运动的功能序列和机制的详细描述。在小型快速跳动的心脏中,瓣膜平面机制由心肌的外部和内部螺旋纤维收缩驱动,这会减小腔室宽度。在收缩期,瓣膜环向心尖下降,心房会扩大。心耳附件必须作为一个补偿储器,使心房壁在心包穹顶内有必要的运动自由度。在这些工作条件下(血容量不足、静脉回流减少),病理生理后果表现为心肌内层相对于中层滑动增加继发的心内膜下出血。心内膜纤维化导致的腔室扩张被解释为心内膜-心包固定逐渐僵硬的结果。这些结构变化逐渐损害了壁厚的收缩-舒张变化。

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