Role of the enteric nervous plexus in rectal motile activity: An experimental study

Citation
A. Shafik et O. El-sibai, Role of the enteric nervous plexus in rectal motile activity: An experimental study, J INVES SUR, 14(5), 2001, pp. 275-281
Citations number
25
Categorie Soggetti
Surgery
Journal title
JOURNAL OF INVESTIGATIVE SURGERY
ISSN journal
08941939 → ACNP
Volume
14
Issue
5
Year of publication
2001
Pages
275 - 281
Database
ISI
SICI code
0894-1939(200109/10)14:5<275:ROTENP>2.0.ZU;2-G
Abstract
The gut innervation is formed by an intrinsic and an extrinsic component. T he former is responsible for the intestinal contractions that occur in the total absence of extrinsic innervation. We hypothesize that the intrinsic p lexuses do not produce local contraction, but mediate re? ex actions of the gut musculature. This hypothesis was investigated in the rectum of the exp erimental animal. In 16 anesthetized mongrel dogs, the rectum was exposed, and 3 monopolar silver-silver chloride electrodes were sutured serially to the rectal wall and connected to a rectilinear pen recorder. The rectal ele ctric activity was recorded at rest and on rectal inflation while the anal pressure was synchronously registered. The tests were repeated after separa te drug administration using phentolamine, propranolol (adrenoceptor blocki ng agents), atropine (cholinergic blocking agent), drotaverine (direct smoo th muscle relaxant), and nitroglycerine. (NO donor, inhibitory noncholinerg ic, nonadrenergic mediator). Slow waves or pacesetter potentials (PPs) and action potentials (APs) were recorded from the three electrodes. Rectal bal loon distension caused an increase of frequency, amplitude, and conduction velocity of these waves, as well as a decrease of anal pressure. Repetition of the test after administration of phentolamine, propranotol, and atropin e effected no change in rectal electromyelographic (EMG) activity or anal p ressure, while drotaverine and nitroglycerine administration aborted both t he electric activity and the anal pressure response. We conclude that the r ectal electric activity, presumably responsible for rectal motility, was no t aborted by enteric nervous plexus block but by direct muscle relaxant. Th is suggests that the enteric plexus has no direct action on the rectal moti le activity but mediates the rectal reflex actions. This concept might expl ain some of the hitherto unknown mechanisms of rectal dyssynergia syndromes .