Zur Interaktion chemosensibler und vagaler Afferenzen auf die respiratorische Moto-Aktivität und die Atemarbeit

Abstract

The central interaction of intracranial and arterial chemoreceptors plays an important role for the generation of respiratory motor activity. Whereas the inspiratory inhibitory effect of lung stretch receptors is largely described, relatively little is known about their influence on expiration and on the pathomechanisms of obstructive airway disease. In anaesthetised cats, electrical activity of inspiratory and expiratory muscles (IM, EM) has been studied along with tidal volume and the position of breathing in eupnoea and increased respiratory drive before and after bilateral vagotomy. In order to mimic slowly adapting lung stretch receptor activity (SAR), the distal ends of vagal nerves (VN) were stimulated electrically using a frequency modulated signal derived from the respiratory alterations in oesophageal pressure. With intact VN, electrical stimulation of carotid sinus nerves or inhalation of 5 % CO (2) in O (2) resulted in an increased activation of IM in inspiration and activation of EM in expiration. Elimination of lung stretch receptor activity during quiet breathing resulted in prolongation and increase in IM activity without much effecting EM, since expiration is passive in eupnoeic breathing. After bilateral vagotomy, the electrical activity of the expiratory muscles was effectively reduced and the activity of the inspiratory muscles was largely enhanced. The effects of vagotomy could be completely reversed by electrical VN stimulation. Simulating an increased tidal volume by increasing the end inspiratory stimulation frequency to more than 100 Hz resulted in a decrease in IM activity and tidal volume. On mimicking an increased end expiratory lung inflation by end expiratory frequencies up to 50 Hz, expiration was prolonged and expiratory muscles activated. In consequence the position of breathing shifted to below the functional residual capacity (FRC). The results of these acute investigations show, that besides terminating inspiration, lung stretch receptors cause a facilitation of expiration during increased respiratory drive and expiratory airflow limitation by activation of expiratory muscles.