Urschel C W, Covell J W, Sonnenblick E H, Ross J, Braunwald E
J Clin Invest. 1968 Apr;47(4):867-83. doi: 10.1172/JCI105780.
The effects on myocardial mechanics of acute, artificial aortic and mitral regurgitation were studied in the dog to determine the manner in which the changes in load induced by valvular regurgitation alter ventricular performance. With mitral and aortic regurgitant volumes of approximately the same magnitude as the forward stroke volume, immediate increases occurred in total stroke volume, left ventricular enddiastolic pressure, and peak ejection velocity, whereas contractility remained unchanged. Although calculated myocardial fiber tension rose, the rate of decline of tension during ejection was accelerated with regurgitation due to the more rapid decrease in ventricular size. Average tension therefore decreased relative to average pressure. As a consequence of the increased fiber length and this unloading, contractile element velocity, work, and power were increased. Despite unchanged contractility of the myocardium, the ejection fraction rose with both aortic and mitral regurgitation.When regurgitant beats were compared with control beats at a constant end-diastolic volume, ventricular stroke volume, work, power, and ejection fraction, as well as contractile element velocity, work, and power consistently increased. Thus, reduction of instantaneous impedance to ejection allowed the ventricle to empty further, reducing ventricular wall tension with a resultant increase in the velocity of shortening. External energy output was increased despite unchanged contractility and diastolic fiber length. It is concluded that the impedance to ejection and myocardial fiber tension during ejection govern the velocity and extent of contractile element shortening, and hence affect stroke volume, peak aortic flow rate, and ejection fraction. The alterations of ventricular function accompanying valvular regurgitation can be explained by an evaluation of the effects of these lesions on the instantaneous impedance to left ventricular ejection.
在犬身上研究了急性人工主动脉瓣和二尖瓣反流对心肌力学的影响，以确定瓣膜反流引起的负荷变化改变心室功能的方式。当二尖瓣和主动脉瓣反流容积与每搏输出量大致相当时，每搏输出总量、左心室舒张末期压力和射血峰值速度立即增加，而收缩性保持不变。尽管计算得出的心肌纤维张力升高，但由于心室大小更快地减小，反流时射血期间张力的下降速率加快。因此，平均张力相对于平均压力降低。由于纤维长度增加和这种负荷减轻，收缩成分的速度、功和功率增加。尽管心肌收缩性不变，但主动脉瓣和二尖瓣反流时射血分数均升高。当在恒定舒张末期容积下将反流搏动与对照搏动进行比较时，心室每搏输出量、功、功率和射血分数，以及收缩成分的速度、功和功率持续增加。因此，射血瞬间阻抗的降低使心室能进一步排空，降低心室壁张力，从而使缩短速度增加。尽管收缩性和舒张期纤维长度不变，但外部能量输出增加。得出的结论是，射血阻抗和射血期间的心肌纤维张力决定收缩成分缩短的速度和程度，从而影响每搏输出量、主动脉峰值流速和射血分数。瓣膜反流伴随的心室功能改变可以通过评估这些病变对左心室射血瞬间阻抗的影响来解释。
