The role of ascending excitatory and descending inhibitory pathways in peristalsis in the isolated guinea-pig small intestine.
AUTOR(ES)
Waterman, S A
RESUMO
1. The effects of experimental manipulations to alter the activation of ascending excitatory and descending inhibitory reflexes on peristalsis were studied in isolated segments of guinea-pig small intestine. 2. The normal site of initiation of the peristaltic contraction, the oral end, was always shifted to a point just anal to a crush which interrupted enteric neuronal pathways. 3. Shortening the functional length of the intestine by a series of crushes, thus effectively reducing the length of enteric neuronal reflex pathways, led to a progressive increase in the threshold distension for triggering the peristaltic contraction. 4. A sleeve placed around the intestine to prevent it from being distended by fluid led to a shift in the site of initiation of the peristaltic contraction to a point just anal to the sleeve. Furthermore, sleeves placed in the anal half of the intestine were able to stop propagation of the contraction. 5. The effect of these manipulations on peristalsis suggests that ascending excitatory and descending inhibitory enteric pathways, activated by distension, determine the pattern of peristaltic activity. The peristaltic contraction is initiated at the oral end as a result of the summation of ascending excitatory inputs and the relative absence of inputs from descending inhibitory pathways at this point. The magnitude of the distension for triggering this contraction is determined by a balance between ascending excitatory and descending inhibitory inputs to the circular muscle. Propagation of the circular muscle contraction requires the activation of ascending excitatory pathways at each point along the intestine and the sequential inactivation of the descending inhibitory reflex pathways anal to the contraction. The propagation of the circular muscle contraction stops when there is no longer a sufficient distension stimulus ahead.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1155880Documentos Relacionados
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