Power spectrum analysis of blood pressure and heart rate and assessment of autonomic nerve activity in knockout mouse

我调查了血压和心率变异性的功率谱分析，当应用于小鼠时，是否提供了关于循环的自主神经控制的有用信息。我发现自回归方法适合于此目的，但必须有效地消除基线的漂移。由此计算的功率谱的特征在于低频（LF）和高频分量（HIF）。通过药理学实验，我证实LF和HF都代表自主神经活动的交感或副交感成分。收缩期动脉压（SAP）变异性的低频成分与交感缩血管神经的活动相对应，心率变异性的低频成分与心交感神经的活动相对应。心率变异性的高频与心脏迷走神经的活动相对应。随后，我将功率谱分析应用于三种类型的基因敲除小鼠。与野生型对应物相比，具有破坏的内皮素基因的敲除小鼠（ET-1敲除小鼠）显示出低约10 mmHg的血压。ET- 1基因敲除小鼠SAP的LF和HF变异性均增加，提示高血压时交感血管神经活动增加。内皮素B（ET B）受体为野生型1/8的基因敲除小鼠（ET B基因敲除小鼠）的血压比野生型小鼠高20 mmHg。而LF和HF在两组间无明显差异，提示ETB基因敲除小鼠的高血压不是神经源性的，而是外周源性的。最后，敲除小鼠缺乏兰尼碱3型受体表现出心率增加和心率变异性的LF和HF减少。这表明心脏迷走神经活动的减少导致这种心动过缓。

I investigated whether the power spectral analysis of blood pressure and heart rate variability, when applied to the mouse, gave useful information on the autonornic nervous control of the circulation. I found that the autoregression method is suitable for this purpose, but that the drift of the baseline had to be effectively removed. The power spectrum thus calculated was characterized by the low (LF) and high frequency components (HIF). By means of pharmacological experiments, I confirmed that both LF and HF represented either sympathetic or parasympathetic component of the autonomic nerve activity. The LF component of systolic arterial pressure (SAP) variability corresponded to activity of sympathetic vasoconstrictor nerve, whereas the LF of heart rate variability represented activity of the cardiac sympathetic nerve. The HF of heart rate variability corresponded to activity of the cardiac vagus nerve. I subsequently applied the power spectral analysis to three types of knockout mice. The knockout mouse with the disrupted endothelin gene (ET-l knockout mouse) showed lower blood pressure by about 10 mmHg as compared to wild type counterparts. Both LF and HF of SAP variability were augmented in ET- 1 knockout mouse indicating elevated activity of sympathetic vasomotor nerve underlay higher blood pressure. In those knockout mice whose endothelin B (ETB) receptors were 1/8 of wild time mice (ETB knockout mice) exhibited higher blood pressure by 20 mmHg than their wild type counterparts. However, no difference m LF and HF were found between the two groups suggesting that high blood pressure of ETB knockout mice was not of neurogenic but peripheral origin. Finally, the knockout mouse lacking ryanodine type 3 receptors showed an increased heart rate and diminished LF and HF of heart rate variability. It is suggested that decrease in cardiac vagal activity caused this bradycardia.