Role of the enteric nervous plexus in rectal motile activity: an experimental study.
The gut innervation is formed by an intrinsic and an extrinsic component. The former is responsible for the intestinal contractions that occur in the total absence of extrinsic innervation. We hypothesize that the intrinsic plexuses do not produce local contraction, but mediate reflex actions of the gut musculature. This hypothesis was investigated in the rectum of the experimental 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 electric activity was recorded at rest and on rectal inflation while the anal pressure was synchronously registered. The tests were repeated after separate drug administration using phentolamine, propranolol (adrenoceptor blocking agents), atropine (cholinergic blocking agent), drotaverine (direct smooth muscle relaxant), and nitroglycerine. (NO donor, inhibitory noncholinergic, nonadrenergic mediator). Slow waves or pacesetter potentials (PPs) and action potentials (APs) were recorded from the three electrodes. Rectal balloon 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 atropine effected no change in rectal electromyelographic (EMG) activity or anal pressure, while drotaverine and nitroglycerine administration aborted both the electric activity and the anal pressure response. We conclude that the rectal electric activity, presumably responsible for rectal motility, was not aborted by enteric nervous plexus block but by direct muscle relaxant. This suggests that the enteric plexus has no direct action on the rectal motile activity but mediates the rectal reflex actions. This concept might explain some of the hitherto unknown mechanisms of rectal dyssynergia syndromes.
Shafik
A
A
Department of Surgery and Experimental Research, Cairo University, Egypt. ashafik@ahmedshafik.org
El-Sibai
O
O
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001683:Biological Clocks / Q000502:physiology; D004285:Dogs; D004576:Electromyography; D017615:Enteric Nervous System / Q000187:drug effects / Q000502:physiology*; D005260:Female; D008297:Male; D009433:Neural Inhibition / Q000502:physiology; D005996:Nitroglycerin / Q000494:pharmacology; D010208:Papaverine / Q000031:analogs & derivatives* / Q000494:pharmacology; D010276:Parasympatholytics / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D012002:Rectal Diseases / Q000503:physiopathology; D012007:Rectum / Q000294:innervation* / Q000502:physiology*; D012018:Reflex / Q000502:physiology
D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D010276:Parasympatholytics; D001285:Atropine; C005317:drotaverin; D011433:Propranolol; D010208:Papaverine; D005996:Nitroglycerin; D010646:Phentolamine