Sensitized central controller of ventilation in rats with chronic heart failure contributes to hyperpnea little at rest but more during exercise.

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 subsystems, i.e., the central controller (arterial CO2 tension [Pa(CO2)] to minute ventilation [V(E)] relationship) and peripheral plant (V(E) to Pa(CO2) 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 Pa(CO2) to V(E) relation. We altered V(E) by varying the level of artificial ventilation and measured the V(E) to Pa(CO2) relation.

RESULTS

Central controller gain S was significantly lager in CHF rats, confirming clinical observation. The V(E) 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 Pa(CO2) 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.