Permanent release of XXXX modulates respiratory frequency in the newborn @entity35 : an in vitro study.

@entity3160 @entity17950 @entity5829 @entity4927 @entity8490 @entity1154 @entity35 @entity669 @entity1063
1. Respiratory activity was recorded on ventral cervical roots during in vitro experiments performed on superfused newborn @entity35 brain stem-cervical cord preparations. 2. Eliminating the pontine structures by performing a transection at the level of the ponto-medullary junction resulted in a sustained increase in respiratory frequency, which suggests the existence of a pontine inhibitory drive impinging on the medullary rhythm generator. 3. @entity1063 (NA) and drugs affecting NA efficiency were added to the bathing medium and the resulting changes in respiratory frequency were analysed. NA decreased the respiratory frequency, and this effect was potentiated by @entity4927 (an inhibitor of the NA degradation by @entity1154 oxidases) and blocked by @entity3160 (an alpha 2-antagonist). 4. @entity3160 or @entity17950 (which blocks the alpha 2-adrenoceptors) increased the resting respiratory frequency to the level reached after ponto-medullary transection, whereas @entity4927 or @entity5829 (which potentiates NA efficiency) decreased the respiratory rate. Since these effects were no longer observed after elimination of the pons, it is suggested that a permanent release of endogenous NA by pontine areas may modulate the activity of the medullary respiratory rhythm generator. 5. When alpha- @entity8490 (an inhibitor of NA biosynthesis) was applied to the pons, the respiratory frequency was increased, whereas when @entity669 (a precursor of NA) was applied, the respiratory frequency decreased. This decrease was enhanced by @entity4927 , suppressed by @entity8490 and blocked by @entity17950 . 6. To conclude, it is suggested that the mechanisms underlying NA biosynthesis (i) continue to function under these in vitro experimental conditions and (ii) are responsible for a permanent release of endogenous NA, which slows down the respiratory frequency. These results are discussed as regards the possibility that the medullary respiratory rhythm generator may be modulated via the noradrenergic area A5 in the newborn @entity35 .
