Cohen Michael A, Taylor J Andrew
Department of Cognitive and Neural Systems, Boston University, Boston, MA, USA.
J Physiol. 2002 Aug 1;542(Pt 3):669-83. doi: 10.1113/jphysiol.2002.017483.
Research into cardiovascular variabilities intersects both human physiology and quantitative modelling. This is because respiratory and Mayer wave (or 10 s) cardiovascular oscillations represent the integrated control of a system through both autonomic branches by systemic haemodynamic changes within a fluid-filled, physical system. However, our current precise measurement of short-term cardiovascular fluctuations does not necessarily mean we have an adequate understanding of them. Empirical observation suggests that both respiratory and Mayer wave fluctuations derive from mutable autonomic and haemodynamic inputs. Evidence strongly suggests that respiratory sinus arrhythmia both contributes to and buffers respiratory arterial pressure fluctuations. Moreover, even though virtual abolition of all R-R interval variability by cholinergic blockade suggests that parasympathetic stimulation is essential for expression of these variabilities, respiratory sinus arrhythmia does not always reflect a purely vagal phenomenon. The arterial baroreflex has been cited as the mechanism for both respiratory and Mayer wave frequency fluctuations. However, data suggest that both cardiac vagal and vascular sympathetic fluctuations at these frequencies are independent of baroreflex mechanisms and, in fact, contribute to pressure fluctuations. Results from cardiovascular modelling can suggest possible sources for these rhythms. For example, modelling originally suggested low frequency cardiovascular rhythms derived from intrinsic delays in baroreceptor control, and experimental evidence subsequently corroborated this possibility. However, the complex stochastic relations between and variabilities in these rhythms indicate no single mechanism is responsible. If future study of cardiovascular variabilities is to move beyond qualitative suggestions of determinants to quantitative elucidation of critical physical mechanisms, both experimental design and model construction will have to be more trenchant.
对心血管变异性的研究涉及人体生理学和定量建模。这是因为呼吸和迈尔波（或10秒）心血管振荡代表了一个充满液体的物理系统内通过自主神经系统的两个分支对系统进行的综合控制，这种控制是由全身血液动力学变化介导的。然而，我们目前对短期心血管波动的精确测量并不一定意味着我们对它们有充分的理解。实证观察表明，呼吸和迈尔波波动都源于可变的自主神经和血液动力学输入。有力证据表明，呼吸性窦性心律不齐既有助于缓冲呼吸性动脉压波动，也会加剧这种波动。此外，尽管通过胆碱能阻滞几乎消除所有R-R间期变异性表明副交感神经刺激对于这些变异性的表达至关重要，但呼吸性窦性心律不齐并不总是反映一种纯粹的迷走神经现象。动脉压力反射被认为是呼吸和迈尔波频率波动的机制。然而，数据表明，这些频率下的心脏迷走神经和血管交感神经波动均独立于压力反射机制，实际上还会导致压力波动。心血管建模结果可以提示这些节律的可能来源。例如，建模最初表明低频心血管节律源于压力感受器控制中的内在延迟，随后的实验证据证实了这种可能性。然而，这些节律之间复杂的随机关系和变异性表明，没有单一机制对此负责。如果未来对心血管变异性的研究要从对决定因素的定性推测转向对关键物理机制的定量阐释，实验设计和模型构建都必须更加精准。
