Vagal contribution to the inspiratory 'off-switch' mechanism.
It has been suggested that vagal contribution to the inspiratory inhibition can be estimated from the difference between the amplitudes of the 'integrated' phrenic activity with and without phasic vagal feedback. At any given body temperature, there is a linear relationship between estimated vagal contribution to the 'off-switch' mechanism and the 'integrated' vagal activity recorded directly. The temperature displaces this relationship to facilitate vagal central effect. There are evidences that a temperature related activity, which is mediated from hypothalamic thermosensitive structures, may directly influence the vagal input to the R beta neurons of the dorsal group of respiratory neurons in the medulla. An increase in Paco2 results in an increase in the peak 'integrated' vagal activity and in the estimated vagal central effect. However, the inhibitory effect of CO2 on pulmonary stretch receptors seems to be enhanced by an increase in body temperature.
D000758:Anesthesia; D000818:Animals; D001831:Body Temperature; D002245:Carbon Dioxide / Q000494:pharmacology*; D002415:Cats; D008465:Mechanoreceptors / Q000502:physiology*; D009433:Neural Inhibition; D010791:Phrenic Nerve / Q000502:physiology; D011661:Pulmonary Stretch Receptors / Q000502:physiology*; D012018:Reflex; D012119:Respiration / Q000187:drug effects; D013990:Tidal Volume; D014630:Vagus Nerve / Q000502:physiology*
D002245:Carbon Dioxide