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PubMed1962

[Pylorospasm].

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Pylorus↗
PubMed1992

Nitric oxide synthase activity in infantile hypertrophic pyloric stenosis.

BACKGROUND: Hypertrophic pyloric stenosis is a common infantile disorder characterized by enlarged pyloric musculature and gastric-outlet obstruction. Its physiopathologic mechanism is not known, but a defect in pyloric relaxation (pylorospasm) has been postulated. Nitric oxide is a mediator of relaxation in the mammalian digestive tract, raising the possibility that pylorospasm could be caused by a defect in nitric oxide production. Since neuronal nitric oxide synthase and NADPH diaphorase are identical, we used the NADPH diaphorase histochemical reaction to study the distribution of nitric oxide synthase in pyloric tissue from patients with infantile hypertrophic pyloric stenosis. METHODS: We studied pyloric tissue from nine infants with infantile hypertrophic pyloric stenosis and seven control infants and children. Cryostat sections were processed for NADPH diaphorase histochemical analysis. A polyclonal tau antiserum was used to identify the enteric nervous system by immunohistochemical methods. RESULTS: NADPH diaphorase activity was restricted to the enteric nervous system and blood vessels. In the pyloric tissues from the control patients, intense diaphorase activity was present in the nerve fibers of the circular musculature, in the neurons and nerve bundles of the myenteric plexus, and in some nerve fibers of the longitudinal musculature. In the pyloric tissues from patients with infantile hypertrophic pyloric stenosis, the enteric nerve fibers in the hypertrophied circular musculature were enlarged and distorted and did not contain diaphorase activity, whereas the activity in the myenteric plexus and the longitudinal musculature was preserved. CONCLUSIONS: We suggest that a lack of nitric oxide synthase in pyloric tissue is responsible for pylorospasm in infantile hypertrophic pyloric stenosis.

Amino Acid Oxidoreductases↗
PubMed1982

Effects of rociverine and other spasmolytic agents on caerulein-induced delay in gastric emptying in the conscious rat.

Caerulein (C)-induced delay in gastric emptying (GE), due to pylorospasm, was used as an experimental model for a quantitative test of the activity of some spasmolytic drugs in conscious rats. Rociverine at doses of 10 and 15 mg kg-1 i.p., though not at higher doses, considerably reduced this delay. Of the other drugs tested only papaverine had this effect and to a lesser degree. Atropine, N-butylscopolammonium bromide and dicyclomine proved to be inactive or further reduced GE. The effect of spasmolytics on C pylorospasm seems to be the outcome of two actions possessed by the drugs in varying degree: on the one hand a pyloric sphincter relaxant action, which increases GE, and on the other a relaxant action on the smooth musculature of the stomach, which tends to reduce GE. The model used highlights the activity of the spasmolytics that act on pylorospasm at doses which per se do not cause a marked delay in GE.

Animals↗
PubMed1986

Pyloric dysfunction in diabetics with recurrent nausea and vomiting.

Diabetes mellitus has been associated with a variety of gastrointestinal motor disturbances. Pyloric activity, however, has not been specifically investigated. We have quantified the pyloric manometric profile in 24 diabetics with recurrent nausea or vomiting, or both, without evidence of mechanical obstruction. Twelve healthy volunteers served as controls. A multilumen pneumohydraulic perfusion assembly with five side openings, each 1 cm apart, was positioned fluoroscopically across the antroduodenal junction and used to monitor pressure activity for 5 h (3 h fasting and 2 h fed). Three patterns of pyloric activity were defined and quantified: (a) baseline elevation of greater than or equal to 3 mmHg for greater than or equal to 1 min (tonic pattern); (b) antral-type phasic pressure activity mixed with duodenal phasic activity (phasic pattern); and (c) phasic pattern superimposed on tonic activity (combined tonic-phasic pattern). The duration of the total pyloric activity before and after the meal was greater in diabetics than in controls (p less than 0.005). Furthermore, episodes of unusually prolonged (greater than or equal to 3 min) and intense (greater than or equal to 10 mmHg) tonic contraction, "pylorospasm," were observed in 14 of 24 diabetics but in only 1 control (p = 0.025). In diabetics, episodes of pylorospasm had a peak amplitude of tonic activity of 13 +/- 1 mmHg and a duration of 7 +/- 0.7 min (mean +/- SE). We conclude that pyloric dysmotility forms part of the widespread disruption of gut motility that affects some patients with diabetes.

Adult↗