Coulshed D S, Hainsworth R, Cowan J C
Academic Department of Clinical Medicine, University of Leeds, United Kingdom.
J Cardiovasc Electrophysiol. 1994 Nov;5(11):919-32. doi: 10.1111/j.1540-8167.1994.tb01132.x.
Contraction-excitation feedback may be an important factor in arrhythmogenesis in patients with heart failure. We have previously demonstrated the contrasting effects of raising left ventricular end-diastolic pressure on action potential duration in dog and guinea pig hearts. The current study was undertaken to assess whether these differing effects might reflect differences in the effect of varying left ventricular end-diastolic pressure on systolic shortening in the two models.
Two models were studied and compared. In open chest dog hearts and isolated guinea pig hearts, measurements of myocardial segment length were made while left ventricular end-diastolic pressure was raised and lowered at constant left ventricular peak systolic pressure. Action potentials were also recorded while left ventricular end-diastolic pressure was changed. The dog hearts were studied further in a manner aimed at reproducing the contraction pattern of the guinea pig hearts. In the in situ dog heart, elevation of left ventricular end-diastolic pressure, and the consequent increase in end-diastolic segment length, was accompanied by a marked increase in systolic shortening, such that minimum systolic segment length remained unchanged. Elevation of left ventricular end-diastolic pressure was accompanied by a prolongation of action potential duration. In the in vitro guinea pig model, elevation of left ventricular end-diastolic pressure was accompanied by more modest changes in systolic shortening, which were not sufficient to compensate for increased diastolic segment length. Consequently, minimum systolic segment length increased as the hearts dilated. Elevation of left ventricular end-diastolic pressure was accompanied by a shortening of action potential duration. In a further series of experiments, the effects of increased left ventricular end-diastolic pressure were studied in the dog model while allowing aortic pressure to rise, thereby restricting systolic shortening. Under these circumstances, the dog model was similar to the guinea pig model, with an increase in left ventricular end-diastolic pressure causing a shortening of action potential duration.
Our results suggest that the effects of preload changes on action potential duration depend on accompanying changes in systolic shortening. This suggests a possible role for contraction-excitation feedback in arrhythmogenesis in patients with regional wall-motion abnormalities.
收缩 - 兴奋反馈可能是心力衰竭患者心律失常发生的一个重要因素。我们之前已经证明，升高左心室舒张末期压力对犬和豚鼠心脏动作电位时程有不同的影响。本研究旨在评估这些不同的影响是否可能反映了在这两种模型中，不同的左心室舒张末期压力对收缩期缩短的影响差异。
对两种模型进行了研究和比较。在开胸犬心脏和离体豚鼠心脏中，在左心室收缩压峰值恒定的情况下，升高和降低左心室舒张末期压力时测量心肌节段长度。同时，在改变左心室舒张末期压力时记录动作电位。对犬心脏进行了进一步研究，旨在重现豚鼠心脏的收缩模式。在原位犬心脏中，左心室舒张末期压力升高以及随之而来的舒张末期节段长度增加，伴随着收缩期缩短的显著增加，使得收缩期最小节段长度保持不变。左心室舒张末期压力升高伴随着动作电位时程的延长。在体外豚鼠模型中，左心室舒张末期压力升高伴随着收缩期缩短的变化较小，不足以补偿舒张期节段长度的增加。因此，随着心脏扩张，收缩期最小节段长度增加。左心室舒张末期压力升高伴随着动作电位时程的缩短。在另一系列实验中，在犬模型中研究了左心室舒张末期压力升高的影响，同时允许主动脉压力升高，从而限制收缩期缩短。在这些情况下，犬模型与豚鼠模型相似，左心室舒张末期压力升高导致动作电位时程缩短。
我们的结果表明，前负荷变化对动作电位时程的影响取决于收缩期缩短的伴随变化。这提示收缩 - 兴奋反馈在局部室壁运动异常患者的心律失常发生中可能起作用。
