The Effect of Respiratory Sinus Arhythmia on the Pulmonary Gas Exchange Efficiency in Humans

呼吸系统和心血管系统的主要功能都是与外部环境和组织交换氧气和二氧化碳。为了实现这一点，这两个系统之间的高度协调，即心肺协调，似乎是从脊椎动物进化的最早阶段发展而来的。迷走神经似乎在这种协调中起着关键作用。心脏迷走神经流出的相性活动与呼吸密切相关，并产生呼吸性窦性心律失常(RSA)。它还会导致吸气时心率增加，呼气时心率减慢，这可能通过在每个呼吸周期中匹配肺毛细血管灌流和肺泡通气量来改善肺气体交换。Hayano等人。结果显示，人工合成的RSA通过降低生理性死腔与潮气量的比率(VDT Phys)和Th…，提高了迷走神经切断犬的气体交换效率静脉内分流率较高。另一方面，肺迷走神经的紧张性活动调节气道平滑肌张力，从而调节解剖死亡空间。我们假设心脏迷走神经的时相性活动和紧张性肺迷走神经的主动活动(分别被估计为呼吸性窦性心律失常和解剖死亡空间体积)有助于提高人体的肺气体交换效率。为了验证这一假设，我们检测了阿托品主动阻断迷走神经对肺气体交换的影响。10名健康志愿者通过安装呼吸分析仪的呼吸回路吸入恒定潮气量和呼吸频率的低氧气体。测量解剖死腔(VDaw)、肺泡死腔(VDalv)和生理性死腔与潮气量的比值(Vd/VT phys)、PaO2和血氧饱和度(SpO2)。记录心电图，以高频成分(0.15~0.2 Hz)R-R间期变异幅度(RRIHF)作为反映呼吸性窦性心律失常(RSA)大小的指标，分别于给药前(对照组)和给药后(0.02 mg/kg)测定肺功能参数。应用阿托品后RRIHF降低(P&lt；0.01)，伴随PaO2和SpO2降低(P&lt；0.05，P&lt；0.01)。应用阿托品后，VDaw、VDalv和Vd/VT phys增加(分别为P&lt；0.01、P&lt；0.05和P&t；0.01)。这些结果与我们的假设是一致的。较少

The primary function of both the respiratory system and the cardiovascular system is to exchange oxygen and carbon dioxide been the external environment and the tissues. To achieve this, a high degree of coordination between these two systems, that is, the cardiorespiratory coordination, seems to have developed from the earliest stages of vertebrate evolution. The vagal nerve system seems to playa key role in this coordination.Phasic activity of the cardiac vagal outflow is closely linked to respiration and produces respiratory sinus arrhythmia (RSA). It also causes increases in heart rate during inspiration and decreases during expiration, which may improve pulmonary gas exchange by matching pulmonary capillary perfusion to alveolar ventilation during each respiratory cycle. Hayano et al. demonstrated that artificially generated RSA improved the efficiency of gas exchange in vagotomized dogs due to the decrease in the ratio of physiological dead space to tidal volume (VDT phys) and th … More e fraction of intrapuhionary shunt. On the other hand, tonic activity ofthe pulmonary vagal nerves regulates airway smooth muscle tone and hence, the anatomical dead space.We hypothesized that both phasic cardiac vagal activity and tonic pulmonary vagal actively, estimated as respiratory sinus arrhythmia and anatomical dead space volume, respectively, contribute to improve the efficiency of pulmonary gas exchange in humans. To test this hypothesis, we examined the effect of blocking vagal nerve actively, achieved with atropine, on pulmonary gas exchange.Ten healthy volunteers inhaled hypoxic gas with constant tidal volume and respiratory frequency through a respiratory circuit in which a respiratory analyzer was installed. Anatomical dead space (VDaw), alveolar dead space (VDalv) and the ratio of physiological dead space and tidal volume (VD/VT phys), Pao2, and oxygen saturation (Spo2) were measured. Electrocardiogram was recorded and the amplitude of R-R interval variability in the high frequency (0.15-0.2 Hz) component (RRIHF) was utilized as an index of respiratory sinus arrhythmia (RSA) magnitude.These parameters of pulmonary function were measured before (control) and after atropine administration (0.02 mg/kg). Decreased RRIHF (P<0.01), as an index of RSA and achieved with atropine administration, was accompanied by the decrease in Pao2 and Spo2 (P<0.05, P<0.01, respectively). VDaw, VDalv, and VD/VT phys increased (P<0.01, P<0.05 and P<0.01, respectively) after atropine administration. These results were consistent with our hypothesis. Less