| Co-Investigator(Kenkyū-buntansha) |
ITO Shoji Nagoya City University, Graduate School of Medical Sciences, Assistant Professor, 大学院・医学研究科, 講師 (40254289)
HAYANO Jun-ichiro Nagoya City University, Graduate School of Medical Sciences, Associate Professor, 大学院・医学研究科, 助教授 (90173054)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 2004: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2003: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Research Abstract |
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
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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
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