Anterior seromyotomy with posterior truncal vagotomy in uncomplicated chronic duodenal ulcer.
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Thirty cases of uncomplicated duodenal ulcer treated by anterior superficial lesser curvature seromyotomy and posterior truncal vagotomy were studied to evaluate the efficacy of this procedure. There was completeness of vagotomy in all the cases as shown by endoscopic Congo Red test. Twenty-seven cases were asymptomatic at 1-48 months (Mean 22.3) follow up, while 3 patients had controllable side effects such as dumping and diarrhoea. There was no mortality. This procedure is safe, effective and is a favourable alternative to highly selective vagotomy. (+info)
Effects of central and peripheral urocortin on fed and fasted gastroduodenal motor activity in conscious rats.
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Since few previous studies have examined the effects of urocortin on physiological fed and fasted gastrointestinal motility, we administered urocortin intracerebroventricularly (icv) or intravenously (iv) in freely moving conscious rats and examined the changes in antral and duodenal motility. Icv and iv injection of urocortin disrupted fasted motor patterns of gastroduodenal motility, which were replaced by fed-like motor patterns. When urocortin was given icv and iv in the fed state, the motor activity remained like the fed patterns but % motor index (%MI) was decreased in the antrum and increased in the duodenum. Increase in the %MI in the duodenum induced by urocortin was shown as a nonpropagated event, since the transit of nonnutrient contents in the duodenum was decreased by icv and iv injection of urocortin. Changes in the gastroduodenal motility induced by icv injection of urocortin were abolished in animals with truncal vagotomy but not altered in animals with mechanical sympathectomy, suggesting that the vagal pathway may mediate the central action of urocortin. Neither urocortin antiserum nor alpha-helical CRF-(9-41) affected fed and fasted gastroduodenal motility, suggesting that endogenous urocortin is not involved in regulation of basal gastroduodenal motility. (+info)
Effect of truncal vagotomy on sphincter of oddi cyclic motility in conscious dogs.
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OBJECTIVE: To evaluate the effects of truncal vagotomy at the diaphragmatic level on the sphincter of Oddi (SO) motility. SUMMARY BACKGROUND DATA: Cholelithiasis is a well-known late complication after gastrectomy and/or vagotomy. The mechanism of gallstone formation is only partly understood, and few studies address the effects of vagotomy on SO cyclic motility in conscious subjects. METHODS: In conscious dogs, SO motility was recorded by retrograde infusion manometry through a duodenal cannula before and after bilateral truncal vagotomy at the diaphragmatic level. Effects of cholecystokinin-octapeptide and feeding were also evaluated before and after vagotomy. RESULTS: SO cyclic motility and the gastroduodenal migrating motor complex continued to occur during postvagotomy fasting. Intermittent inhibitions of the SO and duodenal contractions disappeared during phase 3 of the migrating motor complex. SO basal pressure significantly decreased, whereas the amplitude significantly increased. Cholecystokinin-octapeptide inhibited SO contractions before and after vagotomy. The amplitude of SO contractions increased and their frequency decreased after feeding; however, these effects disappeared after vagotomy. CONCLUSIONS: SO cyclic motility and the effects of feeding change after truncal vagotomy at the diaphragmatic level. These facts may at least partly explain gallstone formation after gastric surgery and/or vagotomy. (+info)
Primary extrapancreatic gastrinoma.
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Extrapancreatic gastrinoma is a rare clinical entity encountered in surgical practice. A patient was referred to us who had a history of recurring symptoms of peptic ulcer disease and ulcer perforation located at an unusual site. Serum gastrin levels were abnormally high. Scopy revealed multiple ulcers in the antrum and duodenum. A mass superior to the head of the pancreas was detected on USG, which later on found to be a separate mass on CT scan. The tumour was excised and confirmed on histopathology. Results of conservative surgery were found to be satisfactory. (+info)
Phytobezoar: an uncommon cause of small bowel obstruction.
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Phytobezoars are an unusual cause of small bowel obstruction. We report 13 patients presenting with 16 episodes of small bowel obstruction from phytobezoars. Eleven patients had previously undergone surgery for peptic ulceration (eight truncal vagotomy and pyloroplasty). A history of ingestion of persimmon fruit was common and the majority of cases presented in the autumn when this fruit is in season. One phytobezoar causing obstruction at the third part of the duodenum was removed by endoscopic fragmentation, while an episode of jejunal obstruction was precipitated by endoscopic fragmentation of a gastric bezoar. Twelve patients underwent surgery for obstruction on 15 occasions, with milking of the phytobezoar to the caecum performed in ten, enterotomy and removal in four and resection in one patient. Associated gastric phytobezoars were found in two cases and multiple small bowel bezoars in two other cases. These were removed to prevent recurrent obstruction. Phytobezoar should be considered preoperatively as a cause of obstruction in patients with previous ulcer surgery. Wherever possible milking of a phytobezoar to the caecum should be performed. Careful assessment for other phytobezoars should be made. Prevention of phytobezoars is dependent upon dietary counselling of patients by surgeons after gastric resection or vagotomy and drainage for peptic ulcer. (+info)
Restraint stress stimulates colonic motility via central corticotropin-releasing factor and peripheral 5-HT3 receptors in conscious rats.
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Although restraint stress accelerates colonic transit via a central corticotropin-releasing factor (CRF), the precise mechanism still remains unclear. We tested the hypothesis that restraint stress and central CRF stimulate colonic motility and transit via a vagal pathway and 5-HT(3) receptors of the proximal colon in rats. (51)Cr was injected via the catheter positioned in the proximal colon to measure colonic transit. The rats were subjected to a restraint stress for 90 min or received intracisternal injection of CRF. Ninety minutes after the administration of (51)Cr, the entire colon was removed, and the geometric center (GC) was calculated. Four force transducers were sutured on the proximal, mid, and distal colon to record colonic motility. Restraint stress accelerated colonic transit (GC of 6.7 +/- 0.4, n=6) compared with nonrestraint controls (GC of 5.1 +/- 0.2, n=6). Intracisternal injection of CRF (1.0 microg) also accelerated colonic transit (GC of 7.0 +/- 0.2, n=6) compared with saline-injected group (GC of 4.6 +/- 0.5, n=6). Restraint stress-induced acceleration of colonic transit was reduced by perivagal capsaicin treatment. Intracisternal injection of CRF antagonists (10 microg astressin) abolished restraint stress-induced acceleration of colonic transit. Stimulated colonic transit and motility induced by restraint stress and CRF were significantly reduced by the intraluminal administration of 5-HT(3) antagonist ondansetron (5 x 10(-6) M; 1 ml) into the proximal colon. Restraint stress and intracisternal injection of CRF significantly increased the luminal content of 5-HT of the proximal colon. It is suggested that restraint stress stimulates colonic motility via central CRF and peripheral 5-HT(3) receptors in conscious rats. (+info)
Importance of the stomach in maintaining calcium homoeostasis in the rat.
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The stomach helps to maintain calcium homoeostasis by making dietary calcium accessible for uptake in the intestines, although the effect of the stomach on calcium homoeostasis is poorly understood. We examined the effect on blood calcium of gastric surgery in the rat. Within three weeks gastrectomy and fundectomy (excision of the acid producing part of the stomach) induced a slight lowering of the blood calcium concentration. When parathyroidectomy was combined with either gastrectomy or fundectomy the blood calcium concentrations promptly dropped to values lower than after parathyroidectomy alone. The mortality was close to 100% during the first three weeks after combined parathyroidectomy and gastric surgery. It was nil in rats subjected to parathyroidectomy alone. Gastrectomised rats absorbed Ca2+ better than unoperated control rats, possibly reflecting the fact that the serum 1,25-dihydroxyvitamin D concentration was raised. Gastrectomised rats had a food intake that was about 70% of that in intact rats, and the amount of dietary calcium absorbed (net absorption per kg body weight) by the gastrectomised rats was approximately 65% of that in intact control rats. We conclude that the acid producing part of the stomach is important for calcium homoeostasis, since its removal induced lethal hypocalcaemia in parathyroidectomised rats. One possible explanation for the hypocalcaemia induced by gastrectomy is a progressive calcium deficit. In addition, the loss of calciotrophic hormones originating in the stomach may contribute. (+info)
Does troncular vagotomy modify the proliferative gastric lesions induced in rats by duodenogastric reflux?
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PURPOSE: to investigate if combining VT to DGR through the pylorus can modulate the biological behavior of PL induced by DGR and to verify if TV alone can induce morphologic lesions in the gastric mucosa. METHODS: 62 male Wistar rats were assigned to four groups: 1 - Control (CT) gastrotomy; 2 - Troncular Vagotomy (TV) plus gastrotomy; 3 - Duodenogastric reflux through the pylorus (R) and 4 - Troncular vagotomy plus DGR (RTV). The animals were killed at the 54 week of the experiment. DGR was obtained by anastomosing a proximal jejunal loop to the anterior gastric wall. TV was performed through isolation and division of the vagal trunks. Gastrotomy consisted of 1 cm incision at the anterior gastric wall. PL were analyzed gross and histologically in the antral mucosa, at the gastrojejunal stoma and at the squamous portion of the gastric mucosa. RESULTS: Groups R and RTV developed exophytic lesions in the antral mucosa (R=90.9%; RTV=100%) and at the gastrojejunal stoma (R=54.54%; RTV=63.63%). Histologically they consisted of proliferative benign lesions, without cellular atypias, diagnosed as adenomatous hyperplasia. Both groups exposed to DGR presented squamous hyperplasia at the squamous portion of the gastric mucosa (R= 54.5%; RTV= 45.4%). TV, alone, did not induce gross or histological alterations in the gastric mucosa. TV did note change the morphologic pattern of the proliferative lesions induced by DGR. CONCLUSIONS: DGR induces the development of PL in the pyloric mucosa and at the gastrojejunal stoma. TV does not change the morphologic pattern of the proliferative lesions induced by DGR. TV alone is not able to induce morphologic lesions in the gastric mucosa. (+info)