Neural mechanisms controlling retrograde giant contraction during vomiting were studied in six conscious dogs with implanted strain gauge force transducers. The small intestine was divided into proximal (P), middle (M), and distal (D) segments. These segments were transplanted on intact mesenteric neurovascular pedicles. In three dogs, M and D segments were interchanged (group A). In three dogs, P and M segments were interchanged (group B). Before transplantation, apomorphine-induced vomiting caused retrograde giant contractions, starting from the M segment and rapidly migrating to the stomach. However, in group A, even after recovery of interdigestive migrating contractions migration, retrograde giant contractions during vomiting always originated in the distally interchanged M segment and jumped to the P segment without migration to the D segment. In group B, the retrograde giant contraction always originated in the proximally interchanged M segment and successively occurred in the distally interchanged P segment. We conclude that origination and migration of retrograde giant contractions are extrinsically controlled. These motor events during vomiting are thought to be a specific motor function that does not exist in the lower small intestine, and retrograde giant contraction during vomiting may originate in the mid-small intestine.
We encountered three cases of chronic functional colonic obstruction caused by intramural ganglion cell death. Morphologic and pharmacological studies were performed using resected specimens. The patients included a 59-year-old man, a 72-year-old woman, and a 28-year-old man. Barium enema studies revealed segmental stenosis in their left colon. A mecholyl test was positive in all three cases and was useful in diagnosing this disorder. Histopathologic and cytometric examinations disclosed both degeneration and the disappearance of intramural ganglion cells. The number of muscarinic acetylcholine receptors was observed to increase in the muscle layers of the stenotic portion. In addition, the muscle of the affected region showed hypersensitivity to the muscarinic agonist (oxotremorine). These results seem to suggest that this disease is caused by a noncongenital injury to the intramural ganglion cells while the resulting stenosis is considered to reflect the degeneration of the ganglion cells. The etiology of ganglion cell death still remains to be clarified; however, we propose that patients with this disorder may represent a subset of patients with sporadic visceral neuropathy.
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