Neural and humoral factors related to diaphragm fatigue

• Main Author: Hall, Neville Huntley
• Format: Dissertation
• Language: English
• Published: University of London 1993

The aim of project was to gain an insight into the neural control of breathing during the development of diaphragm fatigue. In phase one, the role of vagal feedback in the control of breathing during the development of diaphragm fatigue was examined by comparing the ventilatory responses to inspiratory resistive loading (IRL) in vagally intact and vagally denervated rabbits. The results indicate that vagal inputs probably have no significant role to play in the control of breathing during the development of diaphragm fatigue. In phase two, the effects of IRL on arterial blood chemistry were examined to identify noxious chemicals generated during fatiguing IRL. This was necessary to identify potential chemical stimuli of small-phrenic afferent fibres. Potassium was identified as one such stimulus. The increase in arterial potassium concentration ([Ka+]) during IRL was associated with a combined metabolic and respiratory acidosis. On the basis of theoretical considerations, the increase in [K+] could have precipitated diaphragm fatigue. The effects of metabolic and respiratory acidoses on [Ka+] were independently assessed. Both produced a rise in [Ka+], but the sum was less than the rise in [Ka+] produced by IRL. In the final phase, it was established that activation of small-phrenic afferents either by electrical stimulation or by K+ applied to the abdominal surface of the diaphragm caused an increase in minute ventilation and a transient decrease in mean arterial blood pressure. In addition, K+ was shown to excite phrenic afferents. Two patterns of discharge were observed; one was rapidly adapting characteristic of group III fibres, the other was slowly adapting characteristic of group IV fibres.