| Literature DB >> 11834494 |
Nobuko Sasano1, Alex E Vesely, Junichiro Hayano, Hiroshi Sasano, Ron Somogyi, David Preiss, Kiyoyuki Miyasaka, Hirotada Katsuya, Steve Iscoe, Joseph A Fisher.
Abstract
Respiratory sinus arrhythmia (RSA) may improve the efficiency of pulmonary gas exchange by matching the pulmonary blood flow to lung volume during each respiratory cycle. If so, an increased demand for pulmonary gas exchange may enhance RSA magnitude. We therefore tested the hypothesis that CO2 directly affects RSA in conscious humans even when changes in tidal volume (V(T)) and breathing frequency (F(B)), which indirectly affect RSA, are prevented. In seven healthy subjects, we adjusted end-tidal PCO2 (PET(CO2)) to 30, 40, or 50 mmHg in random order at constant V(T) and F(B). The mean amplitude of the high-frequency component of R-R interval variation was used as a quantitative assessment of RSA magnitude. RSA magnitude increased progressively with PET(CO2) (P < 0.001). Mean R-R interval did not differ at PET(CO2) of 40 and 50 mmHg but was less at 30 mmHg (P < 0.05). Because V(T) and F(B) were constant, these results support our hypothesis that increased CO2 directly increases RSA magnitude, probably via a direct effect on medullary mechanisms generating RSA.Entities:
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Year: 2002 PMID: 11834494 DOI: 10.1152/ajpheart.00554.2001
Source DB: PubMed Journal: Am J Physiol Heart Circ Physiol ISSN: 0363-6135 Impact factor: 4.733