The place of pylorus-preserving gastrectomy in the treatment of duodenal ulcer.
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In an attempt to identify the distribution and structure of vagal fibers and terminals in the gastroduodenal junction, vagal efferents were labeled in vivo by multiple injections of the fluorescent carbocyanine dye DiA into the dorsal motor nucleus (dmnX), and vagal afferents were anterogradely labeled by injections of DiI into the nodose ganglia of the same or separate rats. Thick frontal cryostat sections were analysed either with conventional or laser scanning confocal microscopy, using appropriate filter combinations and/or different wavelength laser excitation to distinguish the fluorescent tracers. Vagal efferent terminal-like structures were present in small ganglia within the circular sphincter muscle, which, in the absence of a well-developed, true myenteric plexus at this level, represent the myenteric ganglia. Furthermore, vagal efferent terminals were also present in submucosal ganglia, but were absent from mucosa, Brunner's glands and circular muscle fibers. Vagal afferent fibers and terminal-like structures were more abundant than efferents. The most prominent afferent terminals were profusely branching, large net-like aggregates of varicose fibers running within the connective tissue matrix predominantly parallel to the circular sphincter muscle bundles. Profusely arborizing, highly varicose endings were also present in large myenteric ganglia of the antrum and duodenum, in the modified intramuscular ganglia, and in submucosal ganglia. Additionally, afferent fibers and terminals were present throughout the mucosal lining of the gastroduodenal junction. The branching patterns of some vagal afferents suggested that individual axons produced multiple collaterals in different compartments. NADPH-diaphorase positive, possibly nitroxergic neurons were present in myenteric ganglia of the immediately adjacent antrum and duodenum, and fine varicose fibers entered the sphincter muscle from both sides, delineating the potential vagal inhibitory postganglionic innervation. These morphological results support the view of a rich and differentiated extrinsic neural control of this important gut region as suggested by functional studies.
Acute pancreatitis and leakage of pancreaticojejunal anastomosis are the most important causes of operative morbidity and mortality after pancreatoduodenectomy. We have introduced a modified technique for reconstruction that provides a functional exclusion of the pancreatic-jejunostomy in respect of the transit of gastric and biliary secretions. The immediate advantages of this technique are the reduction in the risk of leakage and the possibility of undertaking conservative treatment, in the case that leakage occurs. The preservation of the antral-pyloric unit, according to Traverso and Longmire, increases the functional features of the procedure, by reducing entero-gastric refluxes, and assuring a regulated gastric emptying. We herein present our series of 11 pancreatoduodenectomies (PD) for periampullary neoplasms and chronic pancreatitis. Throughout our series we experienced no cases of operative mortality. However, there was one specific instance of morbidity, consisting of one case of external biliary fistula by micro-dehiscence of the hepaticjejunostomy and which was later resolved by conservative treatment. Our most recent results have produced almost normal findings in terms of gastric secretion, gastric emptying and an absence of dumping syndrome, ulcers and refluxes.
Pyloric pressure was assayed by a manometric procedure in the basal state and after intraduodenal infusion of HCl. 13 control subjects, 11 patients with benign gastric ulcer, 8 with duodenal ulcer, and 2 with coexistent gastric and duodenal ulcers were studied. Mean resting pyloric pressure in gastric-ulcer patients (5.17 +/- 0.71) mm Hg) was significantly lower than controls (9.40 +/- 0.85 mm Hg) and did not increase after HCl perfusion into the duodenum. Mean basal pyloric pressure in duodenal-ulcer patients (11.30 +/- 1.57 mm Hg) did not differ significantly from controls and increased after intraduodenal perfusion of HCl to 15.72 +/- 2.40 mm Hg. The two patients with coexistent ulcers had manometric patterns similar to gastric-ulcer patients. Decreased pyloric-sphincter pressure in gastric-ulcer patients may be the mechanism responsible for the increased duodeno-gastric reflux observed in these patients.
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Obese Zucker rats are less responsive than their lean littermates to the effects of cholecystokinin-octapeptide on satiety and pancreatic growth and exocrine function. We hypothesized that the hyperphagia observed in obese Zucker rats may be caused by a decreased pyloric contractile response to cholecystokinin, resulting in an increased rate of gastric emptying, decreased postprandial gastric distention, and thus decreased satiety. Pyloric muscle strips from six obese Zucker rats and six lean littermates were mounted in separate tissue baths and isometric contraction was measured in response to acetylcholine and cholecystokinin-octapeptide. The dose-response curves for acetylcholine- and cholecystokinin-octapeptide-stimulated pyloric muscle contraction were similar for both the obese and the lean rats. (For cholecystokinin, D50 obese = 4.0 +/- 0.6 nM, D50 lean = 3.4 +/- 0.2 nM; P = 0.16). We conclude that the decreased satiety response to cholecystokinin-octapeptide observed in obese Zucker rats is not secondary to a decreased pyloric responsiveness to cholecystokinin.