Miyamoto Tadayoshi, Inagaki Masashi, Takaki Hiroshi, Kamiya Atsunori, Kawada Toru, Shishido Toshiaki, Sugimachi Masaru, Sunagawa Kenji
National Cardiovascular Center Res. Inst., Suita, Osaka, Japan.
Conf Proc IEEE Eng Med Biol Soc. 2006;2006:4627-30. doi: 10.1109/IEMBS.2006.260268.
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.
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.
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.
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.
为了解慢性心力衰竭（CHF）运动性通气过度的病理生理基础，我们开发了一种定量表征大鼠通气调节系统的实验方法。平衡图说明了两个子系统的特征，即中央控制器（动脉血二氧化碳分压[Pa(CO2)]与分钟通气量[V(E)]的关系）和外周装置（V(E)与Pa(CO2)的关系）。在本研究中，我们比较了正常大鼠和CHF大鼠静息时的这些指标。
在6只梗死后CHF大鼠和6只正常大鼠麻醉状态下，通过改变吸入二氧化碳分数诱导高碳酸血症，并测量稳态Pa(CO2)与V(E)的关系。通过改变人工通气水平来改变V(E)，并测量V(E)与Pa(CO2)的关系。
CHF大鼠的中央控制器增益S显著更大，证实了临床观察结果。CHF大鼠静息时（工作点）的V(E)大24%；然而，中枢超敏反应对此增加的贡献很小（6%）。
仅中枢超敏反应不能解释CHF大鼠静息时的通气过度。考虑到V(E)与Pa(CO2)关系的右移和上移，中枢超敏反应在运动期间对通气过度的贡献更大。应研究正常大鼠和CHF大鼠在运动诱导的控制器和装置变化方面的潜在差异，以充分了解运动性通气过度的机制并开发减轻这种情况的方法。
