Ishise H, Asanoi H, Ishizaka S, Joho S, Kameyama T, Umeno K, Inoue H
The Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama 930-01, Japan.
J Appl Physiol (1985). 1998 Apr;84(4):1234-41. doi: 10.1152/jappl.1998.84.4.1234.
To elucidate the time course of sympathovagal balance and its relationship to left ventricular function in heart failure, we serially evaluated left ventricular contractility and relaxation and autonomic tone in 11 conscious dogs with tachycardia-induced heart failure. We determined a dynamic map of sympathetic and parasympathetic modulation by power spectral analysis of heart rate variability. The left ventricular peak +dP/dt substantially fell from 3,364 +/- 338 to 1,959 +/- 318 mmHg/s (P < 0.05) on the third day and declined gradually to 1,783 +/- 312 mmHg/s at 2 wk of rapid ventricular pacing. In contrast, the time constant of left ventricular pressure decay and end-diastolic pressure increased gradually from 25 +/- 4 to 47 +/- 5 ms (P < 0.05) and from 10 +/- 2 to 21 +/- 3 mmHg (P < 0.05), respectively, at 2 wk of pacing. The high-frequency component (0.15-1.0 Hz), a marker of parasympathetic modulation, decreased from 1,928 +/- 1,914 to 62 +/- 68 x 10(3) ms2 (P < 0.05) on the third day and further to 9 +/- 12 x 10(3) ms2 (P < 0.05) at 2 wk. Similar to the time course of left ventricular diastolic dysfunction, plasma norepinephrine levels and the ratio of low (0.05- to 0.15-Hz)- to high-frequency component increased progressively from 135 +/- 50 to 532 +/- 186 pg/ml (P < 0.05) and from 0.06 +/- 0.06 to 1.12 +/- 1.01 (P < 0.05), respectively, at 2 wk of pacing. These cardiac and autonomic dysfunctions recovered gradually toward the normal values at 2 wk after cessation of pacing. Thus a parallel decline in left ventricular contractility with parasympathetic influence and a parallel progression in left ventricular diastolic dysfunction with sympathoexcitation suggest a close relationship between cardiac dysfunction and autonomic dysregulation during development of heart failure.
为了阐明心力衰竭时交感 - 迷走神经平衡的时间进程及其与左心室功能的关系，我们连续评估了11只因心动过速诱发心力衰竭的清醒犬的左心室收缩和舒张功能以及自主神经张力。我们通过心率变异性的功率谱分析确定了交感神经和副交感神经调节的动态图谱。左心室峰值 +dP/dt 在第三天从3364±338大幅降至1959±318 mmHg/s（P<0.05），并在快速心室起搏2周时逐渐降至1783±312 mmHg/s。相比之下，左心室压力衰减时间常数和舒张末期压力在起搏2周时分别从25±4逐渐增加至47±5 ms（P<0.05）和从10±2增加至21±3 mmHg（P<0.05）。高频成分（0.15 - 1.0 Hz）是副交感神经调节的标志物，在第三天从1928±1914降至62±68×10³ ms²（P<0.05），并在2周时进一步降至9±12×10³ ms²（P<0.05）。与左心室舒张功能障碍的时间进程相似，血浆去甲肾上腺素水平以及低频（0.05 - 0.15 Hz）与高频成分的比值在起搏2周时分别从135±50逐渐增加至532±186 pg/ml（P<0.05）和从0.06±0.06增加至1.12±1.01（P<0.05）。这些心脏和自主神经功能障碍在起搏停止后2周逐渐恢复至正常值。因此，左心室收缩力与副交感神经影响的平行下降以及左心室舒张功能障碍与交感神经兴奋的平行进展表明，心力衰竭发展过程中心脏功能障碍与自主神经调节异常之间存在密切关系。
