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

基因敲除小鼠血压和心率的功率谱分析及自主神经活动评估

基本信息

批准号：
09670039
负责人：
KUMADA Mamoru
金额：
$ 2.05万
依托单位：
St.Luke's College of Nursing
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1998
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09670039/
关键词：
power spectrum blood pressure electrocardiograph sympathetic nervous system cardiac vagus nerve endothelin-1 gene knockout mouse endothlein B receptor gene knockout mouse ryanodine type3 receptor gene knockout mouse エンドセリン-1 遺伝子欠損マウスノック

项目摘要

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.

我研究了当应用于小鼠时，血压和心率变异性的功率谱分析是否能够提供有关循环的自主神经控制的有用信息。我发现自回归方法适合此目的，但必须有效消除基线的漂移。由此计算出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。收缩动脉压（SAP）变异性的 LF 部分对应于交感血管收缩神经的活动，而心率变异性的 LF 则代表心脏交感神经的活动。心率变异性的 HF 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)表现出血压降低约10mmHg。在 ET-1 敲除小鼠中，SAP 变异性的 LF 和 HF 均增强，表明交感血管舒缩神经活性升高是血压升高的基础。内皮素 B (ETB) 受体为野生型小鼠 1/8 的基因敲除小鼠（ETB 敲除小鼠）的血压比野生型小鼠高 20 mmHg。然而，两组之间的 LF 和 HF 没有发现差异，这表明 ETB 敲除小鼠的高血压不是神经源性的，而是外周起源的。最后，缺乏兰尼碱 3 型受体的基因敲除小鼠表现出心率增加和心率变异性 LF 和 HF 减少。这表明心脏迷走神经活动的减少导致了这种心动过缓。