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是与外界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，似乎已经从脊椎动物进化的最早阶段发展起来。迷走神经系统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）。它还导致在吸气期间心率增加和在呼气期间心率降低，这可以通过在每个呼吸周期期间使肺毛细血管灌注与肺泡通气相匹配来改善肺气体交换。Hayano等人证明，由于生理死腔与潮气量的比值（VDT phys）降低，人工产生的RSA改善了迷走神经切断犬的气体交换效率， ...更多信息 肺内分流率。另一方面，肺迷走神经的紧张性活动调节气道平滑肌张力，因此，解剖死腔。我们假设，无论是阶段性的心脏迷走神经活动和紧张性肺迷走神经积极，估计为呼吸性窦性心律失常和解剖死腔容积，分别有助于提高人类肺气体交换的效率。为了验证这一假设，我们研究了阻断迷走神经积极，实现与阿托品，对肺气体交换的影响。10名健康志愿者吸入低氧气体与恒定的潮气量和呼吸频率通过呼吸回路，其中安装了呼吸分析仪。测量肺动脉解剖死腔（VDaw）、肺泡死腔（VDalv）、生理死腔/潮气量比值（VD/VTphys）、PaO 2、血氧饱和度（Spo 2）。记录心电图，以高频（0.15- 0.2Hz）R-R间期变异幅度（RRIHF）作为呼吸性窦性心律失常（RSA）幅度的指标，分别于对照组和阿托品（0.02mg/kg）给药后测定上述肺功能参数。阿托品组RRIHF下降（P<0.01），Pao 2和Spo 2下降（P<0.05，P<0.01）。阿托品治疗后，VDaw、VDalv和VD/VT phys均明显增加（P<0.01，P<0.05和P<0.01）。这些结果与我们的假设是一致的。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