Proposed respiratory ‘gating’ mechanism for cardiac slowing

Abstract

THREE of the essential variables concerned in the regulation of systemic cardiovascular performance are cardiac output, blood pressure and the resistance encountered by the blood in flowing through the systemic vascular bed. Cardiac output may be further considered as the product of cardiac stroke volume and heart rate. The latter is under the control of the vagi and sympathetic nerves but the reflex bradycardia produced by vagal activation as a result of increased blood pressure, increased carotid chemoreceptor activity or direct electrical stimulation of the carotid sinus nerve occurs only if the stimulus is delivered during expiration. A sustained stimulus which is able reflexly to activate the cardiac vagal efferents will, therefore, produce the pattern of heart rate known as sinus arrhythmia (that is, a slow heart rate regularly interrupted by periods of cardiac acceleration coinciding with inspiration). This association of inspiratory activity with the inhibition of bradycardia is also seen when stimulating certain areas of the brain: areas which produce an inhibition of bradycardia^2,3 also produce an increase in respiratory activity, while other areas produce bradycardia and apnoea⁴. A vagal bradycardia unrelated to respiration can in fact only be induced by stimulating the cells of origin in the nucleus ambiguus^5,6 or the vagus nerve itself. This nucleus lies in the medullary reticular formation ventro-lateral to the nucleus of the tractus solitarius. Since all known afferent stimuli which cause reflex bradycardia converge on the area of the nucleus tractus solitarius where “inspiratory” type neurones abound before passing on to the nucleus ambiguus, it is tempting to postulate that these inspiratory neurones may actually be part of a ‘gate’ which controls the passage of impulses through this reflex pathway. The rhythmical opening and closing of this gate with respiratory activity would result in sinus arrhythmia provided the gate remains open for a sufficient length of time and that there is an adequate background of vagal tone, which is in itself reflexly engendered. We have experimentally analysed some of the properties of this proposed respiratory gating mechanism and conclude that it is in fact influenced by both neural inspiratory activity and by lung inflation.