TY - GEN
T1 - Sensitized central controller of ventilation in rats with chronic heart failure contributes to hyperpnea little at rest but more during exercise
AU - Miyamoto, Tadayoshi
AU - Inagaki, Masashi
AU - Takaki, Hiroshi
AU - Kamiya, Atsunori
AU - Kawada, Toru
AU - Shishido, Toshiaki
AU - Sugimachi, Masaru
AU - Sunagawa, Kenji
PY - 2006
Y1 - 2006
N2 - Background: To understand the pathophysiologic basis of exercise hyperpnea in chronic heart failure (CHF), we have developed an experimental method quantitatively characterizing ventilatory regulation system in rats. An equilibrium diagram illustrates the characteristics of two subsytems, i.e., the central controller (arterial CO2 tension [PaCO2] to minute ventilation [VE] relationship) and peripheral plant (VE to PaCO2 relationship). In this study, we compared these between normal and CHF rats at rest. Method: In anesthetized 6 postinfarction CHF rats and 6 normal rats, we induced hypercapnia by changing inspiratory CO2 fraction and measured the steady-state PaCO2 to VE relation. We altered VE by varying the level of artificial ventilation and measured the VE to PaCO2 relation. Results: Central controller gain S was significantly lager in CHF rats, confirming clinical observation. The VE at rest (operating point) in CHF was 24 % larger; central hypersensitivity, however, contributed little (6 %) to this increase. Conclusion: Central hypersensitivity alone would not explain hyperpnea at rest in CHF rats. Considering the right and upward shift of V E to PaCO2 relation, central hypersensitivity contributes more to hyperpnea during exercise. The potential difference between normal and CHF rats in exercise-induced changes in controller and plant should be examined to fully understand the mechanism of exercise hyperpnea and to develop a method to attenuate this.
AB - Background: To understand the pathophysiologic basis of exercise hyperpnea in chronic heart failure (CHF), we have developed an experimental method quantitatively characterizing ventilatory regulation system in rats. An equilibrium diagram illustrates the characteristics of two subsytems, i.e., the central controller (arterial CO2 tension [PaCO2] to minute ventilation [VE] relationship) and peripheral plant (VE to PaCO2 relationship). In this study, we compared these between normal and CHF rats at rest. Method: In anesthetized 6 postinfarction CHF rats and 6 normal rats, we induced hypercapnia by changing inspiratory CO2 fraction and measured the steady-state PaCO2 to VE relation. We altered VE by varying the level of artificial ventilation and measured the VE to PaCO2 relation. Results: Central controller gain S was significantly lager in CHF rats, confirming clinical observation. The VE at rest (operating point) in CHF was 24 % larger; central hypersensitivity, however, contributed little (6 %) to this increase. Conclusion: Central hypersensitivity alone would not explain hyperpnea at rest in CHF rats. Considering the right and upward shift of V E to PaCO2 relation, central hypersensitivity contributes more to hyperpnea during exercise. The potential difference between normal and CHF rats in exercise-induced changes in controller and plant should be examined to fully understand the mechanism of exercise hyperpnea and to develop a method to attenuate this.
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U2 - 10.1109/IEMBS.2006.260268
DO - 10.1109/IEMBS.2006.260268
M3 - Conference contribution
C2 - 17946641
AN - SCOPUS:34047093372
SN - 1424400325
SN - 9781424400324
T3 - Annual International Conference of the IEEE Engineering in Medicine and Biology - Proceedings
SP - 4627
EP - 4630
BT - 28th Annual International Conference of the IEEE Engineering in Medicine and Biology Society, EMBS'06
T2 - 28th Annual International Conference of the IEEE Engineering in Medicine and Biology Society, EMBS'06
Y2 - 30 August 2006 through 3 September 2006
ER -