Coon R L, Zuperku E J, Kampine J P
J Appl Physiol (1985). 1986 May;60(5):1713-21. doi: 10.1152/jappl.1986.60.5.1713.
The purpose of this study was to determine whether hypocapnia affects heart rate secondary to an effect on pulmonary receptors. Dogs were anesthetized and placed on cardiopulmonary bypass. Interrelationships among airway CO2, central inspiratory activity, and lung receptor effects on respiratory-related heart rate changes (respiratory arrhythmias) were studied after vagal efferent activity was increased secondary to baroreceptor stimulation. Hypocapnia, isolated to the lungs, produced an increase in the magnitude of the respiratory arrhythmias observed. Two mechanisms may produce these results. Hypocapnia affects pulmonary receptors, which 1) reflexly alter heart rate and 2) modulate breathing frequency, thus altering the dynamics of the respiratory arrhythmias that were produced. The results also suggested that the reflex increase in heart rate in response to lung inflation and the Hering-Breuer expiratory-facilitatory reflex are either produced by different pulmonary receptors or by the same pulmonary receptors but may be mediated by different central mechanisms.
本研究的目的是确定低碳酸血症是否通过对肺受体的影响继发地影响心率。对狗进行麻醉并置于体外循环。在压力感受器刺激继发迷走神经传出活动增加后,研究气道二氧化碳、中枢吸气活动和肺受体对呼吸相关心率变化(呼吸性心律失常)的相互关系。仅作用于肺部的低碳酸血症使观察到的呼吸性心律失常的幅度增加。可能有两种机制产生这些结果。低碳酸血症影响肺受体,其一是反射性地改变心率,其二是调节呼吸频率,从而改变所产生的呼吸性心律失常的动态变化。结果还表明,对肺扩张的心率反射性增加和黑林 - 布雷尔呼气易化反射要么由不同的肺受体产生,要么由相同的肺受体产生,但可能由不同的中枢机制介导。