Shea S A, Andres L P, Shannon D C, Guz A, Banzett R B
Physiology Program, Harvard School of Public Health, Boston, Massachusetts 02115.
Respir Physiol. 1993 Aug;93(2):203-19. doi: 10.1016/0034-5687(93)90006-v.
An urge to breath is perceived during breath hold and hypercapnia (termed 'air hunger') and during heavy exercise (often termed 'shortness of breath'). To better understand the neural mechanisms responsible for these sensations we studied five patients (8-17 years old) with congenital central hypoventilation syndrome (CCHS) who lack ventilatory response to CO2. CCHS patients reported no respiratory discomfort during CO2 inhalation or during maximal breath hold which was of much longer duration than age-matched controls. However, all 3 CCHS patients who exercised heavily reported some sensations akin to shortness of breath (they increased breathing nearly as much as controls). Our results are consistent with two possibilities. First, the air hunger of hypercapnia and breath hold is caused by projection to the forebrain of respiratory chemoreceptor afferents which bypass the respiratory centers, while exercise shortness of breath is caused by direct projections of limb afferents or locomotory center activity. Second, air hunger and shortness of breath share the same origin--projection of increased brain stem respiratory center motor activity (corollary discharge) to the forebrain.
在屏气和高碳酸血症期间（称为“空气饥饿”）以及剧烈运动期间（通常称为“呼吸急促”）会感觉到呼吸冲动。为了更好地理解产生这些感觉的神经机制，我们研究了五名患有先天性中枢性低通气综合征（CCHS）的患者（8 - 17岁），他们对二氧化碳缺乏通气反应。CCHS患者在吸入二氧化碳期间或最大屏气期间（其持续时间比年龄匹配的对照组长得多）未报告呼吸不适。然而，所有3名进行剧烈运动的CCHS患者都报告了一些类似于呼吸急促的感觉（他们的呼吸增加程度与对照组几乎相同）。我们的结果符合两种可能性。第一，高碳酸血症和屏气时的空气饥饿是由呼吸化学感受器传入神经投射到前脑引起的，这些传入神经绕过了呼吸中枢，而运动性呼吸急促是由肢体传入神经的直接投射或运动中枢活动引起的。第二，空气饥饿和呼吸急促有共同的起源——脑干呼吸中枢运动活动增加（伴随放电）投射到前脑。
