[HTML][HTML] Nitric oxide synthase activity in infantile hypertrophic pyloric stenosis

JM Vanderwinden, P Mailleux… - … England Journal of …, 1992 - Mass Medical Soc
JM Vanderwinden, P Mailleux, SN Schiffmann, JJ Vanderhaeghen, MH De Laet
New England Journal of Medicine, 1992Mass Medical Soc
Background Hypertrophic pyloric stenosis is a common infantile disorder characterized by
enlarged pyloric musculature and gastric-outlet obstruction. Its physio-pathologic
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 …
Background
Hypertrophic pyloric stenosis is a common infantile disorder characterized by enlarged pyloric musculature and gastric-outlet obstruction. Its physio-pathologic 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. (N Engl J Med 1992;327:511–5.)
The New England Journal Of Medicine