WALL STRESS-INDUCED ARRHYTHMIA IS ENHANCED BY LOW POTASSIUM AND EARLY LEFT-VENTRICULAR HYPERTROPHY IN THE WORKING RAT-HEART
WALL STRESS-INDUCED ARRHYTHMIA IS ENHANCED BY LOW POTASSIUM AND EARLY LEFT-VENTRICULAR HYPERTROPHY IN THE WORKING RAT-HEART
复制标题
DOI：
10.1016/s0008-6363(96)88534-8
复制
发表时间：
1995-04-01
影响因子：
10.8
通讯作者：
JONES, JV
中科院分区：
文献类型：
--
作者：
EVANS, SJ;LEVI, AJ;JONES, JV
目的：目的是研究降低外部钾对正常和肥大大鼠心脏对室壁应力增加引起的心律失常的敏感性的影响。研究方法：采用离体工作心脏模型，比较自发性高血压大鼠（SHR）与Wistar和Wistar-Kyoto品系血压正常对照大鼠（NCR）的肥厚心脏。使用年幼动物[131.5（SEM 0.64）天]以确保无并发症的左心室肥大。室壁应力增加20 s诱发心律失常。记录心电图，并在用含[K] 6、4.8、3.6和2.4 mM的Tyrode溶液灌注期间比较每个心脏的心律反应。当用[K] 3.6和2.4 mM灌注时，在所有水平的后负荷增加下，肥大的SHR心脏显示出比对照心脏明显更大的心律失常反应t检验P < 0.05和P < 0.01。SHR心脏心律失常的数量和复杂性均增加;室性心动过速发生在10/12与4/12的对照心脏相比，而室颤发生在5/12的心脏，但在对照心脏中没有。结论：在高[K]水平时，SHR心脏与正常心脏对室壁应激性心律失常的敏感性相似。然而，当[K]降低到3.6 mM或更低时，肥厚心脏对心室壁应力增加的反应大大增强，与正常心脏相比，它们会发生更多的心室异位和更复杂的室性心律失常。这可能与左心室肥厚、钾耗竭和血压不稳定的高血压患者的猝死有关。收缩压的过度波动以及由此引起的心室壁应力可为伴有左心室肥大的高血压患者提供强大的心肌刺激，甚至在缺血、心力衰竭或广泛的细胞外纤维化发生之前。
Objective: The aim was to investigate the effect of lowering external potassium on the sensitivity of the normal and hypertrophied rat heart to arrhythmias induced by increases in ventricular wall stress. Methods: The isolated working heart model was used to compare hypertrophied hearts from the spontaneously hypertensive rat (SHR) with hearts from normotensive control rats (NCR) from the Wistar and Wistar-Kyoto strains. Young animals [131.5(SEM 0.64) days] were used to ensure uncomplicated left ventricular hypertrophy. Arrhythmias were induced by 20 s increases in ventricular wall stress. The ECG was recorded and the al-rhythmic response of each heart was compared during perfusion with Tyrode solutions containing [K] 6, 4.8, 3.6, and 2.4 mM. Results: Hypertrophied SHR hearts showed a significantly greater arrhythmic response than control hearts at all levels of afterload increase when perfused with [K] 3.6 and 2.4 mM (t test P < 0.05 and P < 0.01). Both the number and complexity of arrhythmias were increased in the SHR hearts; ventricular tachycardia occurred in 10/12 compared with 4/12 control hearts whereas ventricular fibrillation occurred in 5/12 hearts but in none of the control hearts. Conclusions: At higher levels of [K] the sensitivity of SHR hearts and normal hearts to wall stress induced arrhythmias is similar. However, as [K] is lowered to 3.6 mM or below, hypertrophied hearts show a greatly enhanced response to increases in ventricular wall stress They develop a larger number of ventricular ectopics and more complex ventricular arrhythmias when compared to normal hearts. This may be of relevance to arrhythmic sudden death in hypertensive patients in whom left ventricular hypertrophy, potassium depletion, and blood pressure lability is common. Excessive fluctuations in systolic pressure and therefore ventricular wall stress could provide a powerful arrhythmic stimulus in hypertensive patients with left ventricular hypertrophy, even before ischaemia, cardiac failure, or extensive extracellular fibrosis have developed.