James M A, Jones J V
Department of Cardiology, Bristol Royal Infirmary, UK.
J Hypertens. 1992 Feb;10(2):167-72. doi: 10.1097/00004872-199202000-00010.
To investigate the interrelationship between arrhythmias provoked by acute pressure changes, and the presence of left ventricular hypertrophy and electrolyte imbalances.
An isolated working rat heart model was used in a prospective comparison of the effects of acute pressure changes in hypertensive and normotensive hearts during perfusion with perfusate containing differing electrolyte compositions.
An experimental laboratory study. STUDY MATERIALS: Forty-four rat hearts (20 hypertensive, 24 normotensive).
Hearts were subjected to sudden pressure changes of varying sizes during perfusion with two different electrolyte solutions and the arrhythmias provoked were recorded.
The size of the pressure change necessary to provoke arrhythmias, and the amount and severity of arrhythmias provoked by equivalent-sized pressure changes.
During perfusion with normal electrolyte concentrations, no hypertrophied hearts developed arrhythmia compared with more than half of the normal hearts during equivalent-sized pressure changes, and a much larger pressure increase was necessary to produce any arrhythmia in the hypertrophied hearts. During perfusion with cation-depleted perfusate, arrhythmias significantly increased in both groups of hearts, but the pattern was reversed; more than half of the hypertrophied hearts compared with none of the normal hearts developed ventricular tachycardia during equivalent-sized pressure increases, whilst the minimum pressure change necessary to provoke arrhythmia became significantly smaller in the hypertrophied hearts compared with the normal hearts.
Left ventricular hypertrophy plays a paradoxical role in the development of arrhythmias in this model. It appears to protect the heart from developing arrhythmias in response to sudden pressure changes when electrolyte concentrations are normal. However, it also seems to lead to a marked increase in the sensitivity of the myocardium to pressure changes during perfusion with low levels of potassium and magnesium. Under these conditions, potentially fatal arrhythmias can be readily provoked by relatively small pressure changes. These results may be of importance for the management of hypertension and may provide insight into some of the mechanisms underlying sudden death in hypertension. The findings may also be of relevance to other cardiac diseases associated with ventricular hypertrophy or abnormal wall stress.
研究急性压力变化诱发的心律失常与左心室肥厚及电解质失衡之间的相互关系。
采用离体工作大鼠心脏模型，前瞻性比较在灌注含不同电解质成分的灌注液时，高血压和正常血压心脏中急性压力变化的影响。
一项实验性实验室研究。研究材料：44只大鼠心脏（20只高血压心脏，24只正常血压心脏）。
在用两种不同电解质溶液灌注期间，使心脏承受不同大小的突然压力变化，并记录诱发的心律失常。
诱发心律失常所需的压力变化大小，以及同等大小压力变化诱发的心律失常的数量和严重程度。
在正常电解质浓度灌注期间，与同等大小压力变化时超过一半的正常心脏相比，没有肥厚心脏发生心律失常，并且肥厚心脏产生任何心律失常都需要更大的压力升高。在用阳离子缺乏的灌注液灌注期间，两组心脏的心律失常均显著增加，但模式相反；在同等大小的压力升高期间，超过一半的肥厚心脏发生室性心动过速，而正常心脏无一发生，同时与正常心脏相比，肥厚心脏诱发心律失常所需的最小压力变化显著变小。
在该模型中，左心室肥厚在心律失常的发生中起矛盾作用。当电解质浓度正常时，它似乎能保护心脏免受突然压力变化诱发的心律失常。然而，在低钾和低镁灌注期间，它似乎也会导致心肌对压力变化的敏感性显著增加。在这些情况下，相对较小的压力变化就很容易诱发潜在致命的心律失常。这些结果可能对高血压的治疗具有重要意义，并可能为高血压猝死的一些潜在机制提供见解。这些发现也可能与其他与心室肥厚或异常壁应力相关的心脏病有关。
