Ng G A, Cobbe S M, Smith G L
Department of Medical Cardiology, University of Glasgow, UK.
Cardiovasc Res. 1998 Feb;37(2):489-502. doi: 10.1016/s0008-6363(97)00255-1.
To study the time course of Ca2+ transients recorded from the left ventricular epicardial surface of isolated hearts from rabbits with heart failure and to correlate the results with mechanical function.
Heart failure was induced in the rabbit 8 weeks after coronary ligation (n = 17) with 13 controls. Echocardiography was used to assess in vivo left ventricular dysfunction. The fluorescent indicator Indo-1 was loaded into isolated Langendorff-perfused hearts and Ca2+ transients were recorded from 15 sites over the left ventricular epicardial surface using a single core light guide. The time course of the Ca2+ transients was analysed and the duration measured and correlated with in vitro mechanical function.
Significant mechanical dysfunction was produced in this model of heart failure. The mean duration of the Ca2+ transients obtained from failing hearts was prolonged (156.2 +/- 3.2 ms) when compared to controls (124.9 +/- 2.6 ms, P < 0.001). Delayed relaxation as measured by the maximum rate of intraventricular pressure decay was significantly correlated with the prolonged Ca2+ transients (r = -0.63, P < 0.001). In addition, there was increased variation of the Ca2+ transient duration in the failing hearts.
Coronary artery ligation-induced heart failure is associated with changes in the surviving myocardium which result in a non-uniform prolongation of Ca2+ transient duration. This suggests that there is a regional heterogeneity to the abnormal intracellular Ca2+ handling in heart failure.
研究从心力衰竭家兔离体心脏左心室心外膜表面记录的Ca2+瞬变的时程，并将结果与机械功能相关联。
在冠状动脉结扎8周后诱导家兔发生心力衰竭（n = 17），另有13只作为对照。采用超声心动图评估体内左心室功能障碍。将荧光指示剂Indo-1加载到离体Langendorff灌注心脏中，使用单芯光导从左心室心外膜表面的15个部位记录Ca2+瞬变。分析Ca2+瞬变的时程，测量其持续时间，并与体外机械功能相关联。
该心力衰竭模型产生了明显的机械功能障碍。与对照组（124.9±2.6毫秒，P < 0.001）相比，衰竭心脏获得的Ca2+瞬变的平均持续时间延长（156.2±3.2毫秒）。以心室内压最大下降速率测量的延迟舒张与延长的Ca2+瞬变显著相关（r = -0.63，P < 0.001）。此外，衰竭心脏中Ca2+瞬变持续时间的变化增加。
冠状动脉结扎诱导的心力衰竭与存活心肌的变化有关，这些变化导致Ca2+瞬变持续时间不均匀延长。这表明心力衰竭时细胞内Ca2+处理异常存在区域异质性。
