effects of cold block of the spinal cord in respiratory movement during hypocapnic apnoea

ABSTRACT

This paper investigates at segmental level, the behaviour of respiratory motorneurones during cold blocking of the spinal cord in hypocapnic apnoea. In expiratory biased preparations, lowering CO[2] level renders the inspiratory motoneurones silent, whereas the expiratory motorneurones discharge tonically. As for the effects of cold stimuli in eupnoea, application of the cold thermode to the dorsolateral surface of the spinal cord in hypocapnic apnoea evoked transient reciprocal reflex burst activity of both inspiratory and expiratory motoneurone populations. The expiratory burst activity attained double that of the control level. These activities could be explained by same reasoning as for dorsolateral cold block of the spinal cord in eupnea. Alternatively this additional activity may be attributed to the tonic non-respiratory source. Following recovery from blocking, the expiratory motoneurones showed an exaggerated tonic activity mounting double that before blocking and at the same level of the excitatory response produced by the cold thermode. The simplest explanation of this additional activity would be that, the effects of cold thermode could have aroused the preparation and over the time scale involved nearly 30min; led to a lighter level of general anaesthesia which would favour the expiratory bias state of the preparation. Alternatively, a release process was involved. An interesting possibility could be that, this exaggerated expiratory activity could have resulted from postsynaptic potentiation induced by accumulation of synaptic transmitter following cold block of the expiratory bulbospinal drive. Another possibility could be due to another system whose activity was released by blocking. One candidate for this would be the reticulospinal fibres arising from the nucleus reticularis gigantocellularis. Because sustained stimulation within the medial reticular formation causes a sustained activation of expiratory motoneurons and reciprocal inhibition of inspiratory motoneurons. Hence, it is proposed that such added tonicity of discharge arises from released traffic in the reticulospinal and expiratory bulbospinal axons