Ito Shoji, Sasano Hiroshi, Sasano Nobuko, Hayano Junichiro, Fisher Joseph A, Katsuya Hirotada
Department of Anaesthesiology and Medical Crisis Management, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467-8601, Japan.
Exp Physiol. 2006 Sep;91(5):935-41. doi: 10.1113/expphysiol.2006.034421. Epub 2006 Jun 29.
The aim of this study was to test our hypothesis that both phasic cardiac vagal activity and tonic pulmonary vagal activity, estimated as respiratory sinus arrhythmia (RSA) and anatomical dead space volume, respectively, contribute to improve the efficiency of pulmonary gas exchange in humans. We examined the effect of blocking vagal nerve activity with atropine on pulmonary gas exchange. Ten healthy volunteers inhaled hypoxic gas with constant tidal volume and respiratory frequency through a respiratory circuit with a respiratory analyser. Arterial partial pressure of O(2) (P(aO(2))) and arterial oxygen saturation (S(pO(2))) were measured, and alveolar-to-arterial P(O(2)) difference (D(A-aO(2))) was calculated. Anatomical dead space (V(D,an)), alveolar dead space (V(D,alv)) and the ratio of physiological dead space to tidal volume (V(D,phys)/V(T)) were measured. Electrocardiogram was recorded, and the amplitude of R-R interval variability in the high-frequency component (RRIHF) was utilized as an index of RSA magnitude. These parameters of pulmonary function were measured before and after administration of atropine (0.02 mg kg(-1)). Decreased RRIHF (P < 0.01) was accompanied by decreases in P(aO(2)) and S(pO(2)) (P < 0.05 and P < 0.01, respectively) and an increase in D(A-aO(2)) (P < 0.05). Anatomical dead space, V(D,alv) and V(D,phys)/V(T) increased (P < 0.01, P < 0.05 and P < 0.01, respectively) after atropine administration. The blockade of the vagal nerve with atropine resulted in an increase in V(D,an) and V(D,alv) and a deterioration of pulmonary oxygenation, accompanied by attenuation of RSA. Our findings suggest that both phasic cardiac and tonic pulmonary vagal nerve activity contribute to improve the efficiency of pulmonary gas exchange in hypoxic conscious humans.
本研究的目的是检验我们的假设，即分别以呼吸性窦性心律不齐（RSA）和解剖无效腔容积估算的心脏迷走神经的相位活动和肺迷走神经的紧张性活动，有助于提高人类肺气体交换的效率。我们研究了用阿托品阻断迷走神经活动对肺气体交换的影响。10名健康志愿者通过带有呼吸分析仪的呼吸回路，以恒定潮气量和呼吸频率吸入低氧气体。测量动脉血氧分压（P(aO₂)）和动脉血氧饱和度（S(pO₂)），并计算肺泡-动脉血氧分压差（D(A-aO₂)）。测量解剖无效腔（V(D,an)）、肺泡无效腔（V(D,alv)）以及生理无效腔与潮气量的比值（V(D,phys)/V(T)）。记录心电图，高频成分的R-R间期变异性幅度（RRIHF）用作RSA大小的指标。在给予阿托品（0.02 mg kg⁻¹）之前和之后测量这些肺功能参数。RRIHF降低（P < 0.01）的同时，P(aO₂)和S(pO₂)降低（分别为P < 0.05和P < 0.01），D(A-aO₂)升高（P < 0.05）。给予阿托品后，解剖无效腔、V(D,alv)以及V(D,phys)/V(T)增加（分别为P < 0.01、P < 0.05和P < 0.01）。用阿托品阻断迷走神经导致V(D,an)和V(D,alv)增加以及肺氧合恶化，并伴有RSA减弱。我们的研究结果表明，心脏迷走神经的相位活动和肺迷走神经的紧张性活动均有助于提高低氧清醒人类的肺气体交换效率。
