There is substantial experimental and anatomic evidence suggesting that the human lower esophageal sphincter is not a muscular ring but has its correlate in the arrangement of the so-called muscular clasps and oblique sling fibers at the gastroesophageal junction. We assessed the mode of action of these distinct muscle units in a mechanical model. The arrangement of the clasp and sling fibers at the gastroesophageal junction was simulated with two elastic bands placed perpendicularly around the gastroesophageal junction of four pig specimens. Rapid pullback manometry with four radially oriented pressure transducers was performed in each specimen. The opening pressure was determined, and three-dimensional pressure images were constructed based on the manometric readings. The elastic bands established a competent high-pressure zone at the level of the gastroesophageal junction. The three-dimensional pressure images matched those usually observed in vivo in normal human volunteers. The vector volume of the high-pressure zone correlated with the opening pressure while individual resting pressure values and length of the high-pressure zone were not sufficient to estimate the competence of the gastroesophageal junction in the model. This model supports the contention that the combined action of the clasp and sling fibers establishes the manometric lower esophageal sphincter in humans.
Impaired gastric emptying in gastric ulcer patients has generally been explained by gastric hypomotility. The gastric motor response to an electrical vagal stimulus was measured intraoperatively in patients with gastric ulcers (GU, n = 21), duodenal ulcers (DU, n = 25) and combined ulcers (GDU, n = 6). Amplitude and duration of the contraction and integrated motor response were found to be significantly greater in GU patients than in patients with duodenal and combined ulcers. Thus, hypermotility of the gastric muscle exists in GU patients and the delayed gastric emptying in GU disease may be the result of antropyloric motor dysfunction rather than of gastric hypotony. Abnormal motility associated with duodenogastric reflux appears to be a key feature in the pathogenesis of gastric ulcer.
In a prospective multicenter trial, 560 patients with peptic ulcer were treated with proximal gastric vagotomy (PGV) without drainage. Four hundred ninety-three patients had duodenal ulcer (DU), 35 pyloric (PU), and 32 prepylorlc ulceration (PPU). Actuarial 5-year recurrence rates were 14%, 35 %, and 33%, respectively, and were significantly higher in PU and PPU than in DU. In a separate study, thickness of the pyloric and antrai wail was assessed in the resection specimens of patients with similarly defined ulcer types and in controls. There was significant thickening of the muscular layer of the pylorus and antrum in patients with PU and PPU compared to those with DU and controls. It appears that this muscular hypertrophy and fibrosis could be one factor responsible for the failure of PGV without drainage in PU and PPU. Preliminary results indicate a possible beneficial effect of adding a drainage procedure ~o PGV when treating pyloric channel ulcers. Our results emphasize that pyloric channel ulcers must be considered as a particular entity of peptic ulcer disease and should no longer be assigned to the duodenal ulcer group.
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