Madwed J B, Cohen R J
Department of Physiology, Harvard Medical School, Harvard-Massachusetts Institute of Technology, Boston 02115.
Am J Physiol. 1991 Apr;260(4 Pt 2):H1248-53. doi: 10.1152/ajpheart.1991.260.4.H1248.
We have previously reported that oscillations at 0.05 Hz can be generated by a simple computer model incorporating a negative-feedback reflex mechanism and an effector mechanism with a time delay. Computer simulations by inhibiting the vagal effector mechanism and activating the adrenergic effector mechanism elicited low-frequency oscillations at a frequency of 0.05 Hz in heart rate. We have observed that the cardiovascular system of the conscious dog, when stressed by the loss of blood, generates oscillations in arterial pressure and heart rate at a frequency of 0.05 Hz. We investigated in six conscious dogs the role of the sympathetic and parasympathetic nervous systems in generating these heart rate oscillations. During baseline conditions, the predominant peak in the arterial pressure and heart rate power spectra was located at the respiratory frequency, while the low-frequency oscillations were small. After a 30-ml/kg hemorrhage or after an 8-, 15-, or 30-ml/kg hemorrhage with glycopyrrolate, a muscarinic-blocking agent, low-frequency oscillations at a frequency of 0.05 Hz predominated, while the respiratory frequency oscillations were negligible. Since respiratory frequency oscillations have been reported to reflect vagal activity, and since the low-frequency oscillations were present after vagal blockade, these hemorrhage-induced low-frequency oscillations in heart rate may be primarily mediated by the cardiac sympathetic nerves. Also cross-correlation analysis between arterial pressure and heart rate showed that a change in arterial pressure caused an opposite change in heart rate with a delay of 2-5 s. We conclude that hemorrhage-induced oscillations in heart rate at 0.05 Hz represent the arterial baroreceptor-beta-sympathetic reflex response to underlying arterial pressure oscillations.
我们之前曾报道，通过一个包含负反馈反射机制和具有时间延迟的效应器机制的简单计算机模型，可以产生0.05赫兹的振荡。通过抑制迷走神经效应器机制并激活肾上腺素能效应器机制进行的计算机模拟，引发了心率以0.05赫兹频率的低频振荡。我们观察到，清醒犬的心血管系统在失血应激时，会产生动脉血压和心率以0.05赫兹频率的振荡。我们在六只清醒犬中研究了交感神经系统和副交感神经系统在产生这些心率振荡中的作用。在基线条件下，动脉血压和心率功率谱中的主要峰值位于呼吸频率处，而低频振荡较小。在30毫升/千克失血后，或在使用毒扁豆碱（一种毒蕈碱阻断剂）进行8、15或30毫升/千克失血后，以0.05赫兹频率的低频振荡占主导，而呼吸频率振荡可忽略不计。由于据报道呼吸频率振荡反映迷走神经活动，且在迷走神经阻断后出现低频振荡，这些失血诱导的心率低频振荡可能主要由心脏交感神经介导。此外，动脉血压与心率之间的互相关分析表明，动脉血压的变化会导致心率在延迟2至5秒后出现相反的变化。我们得出结论，失血诱导的0.05赫兹心率振荡代表了对潜在动脉血压振荡的动脉压力感受器 - β - 交感神经反射反应。
