The proximal gastric vagotomy in the treatment of uncomplicated duodenal ulcer (author's transl)]

Of 97 patients, who had a PGV since July 1971, 86 were checked intraoperatively on completeness of vagotomy with various methods, including Kongo-red-staining, pH-electrode and Burge-test. On theoretical grounds, the Burge-test combined with pH-measurement seems the most reliable procedure. In 14 cases an incomplete Vagotomy could such be avoided. 72 patients, who met the critiria of more than 6 months follow-up, were graded according to VISICK with 89% good results (I, II) and 11% VISICK III, IV. Two Patients needed reoperation, one with recurrent ulcer. Our results confirm the good impression we had initially, regarding the low postoperative morbidity, effective reduction of acidity and recurrence rate, but longterm follow-up studies are still required to form a final judgement.     

Expedient surgical treatment of chronic ulcer stenosis. A case for proximal gastric vagotomy

Forty-nine patients with chronic pyloroduodenal ulcer stenosis were treated surgically in our hospitals between 1977 and 1985. Three operations were used: 16 patients had a proximal gastric vagotomy-pyloroplasty (PGV-P); 26 had a vagotomy-antrectomy (V-A); and seven had a truncal vagotomy-pyloroplasty (TV-P). Historical data and preparations for operation were similar in each group. We compared the early clinical outcome in these patients. Two patients died after V-A and one died after TV-P. Five patients were reoperated: V-A (three patients), PGV-P and TV-P (one patient each). Delayed gastric emptying with nonoperative resolution (DGE) occurred in nine patients after V-A and in two patients after TV-P. Preoperative gastric suction and parenteral nutrition did not avoid DGE or affect timing of return to a general diet. A solid diet was resumed earlier (p less than 0.01) after PGV-P (5 +/- 1 days) than after V-A (13 +/- 8 days) or TV-P (9 +/- 2 days). Ninety-four percent of patients after PGV-P had an uneventful recovery, compared with 46 and 43% after V-A and TV-P, respectively. Among the variables measured, operative choice of PGV-P expedited early surgical recovery of patients with chronic ulcer stenosis.     

Dysphagia after proximal gastric vagotomy.

Ten patients were examined before and after proximal gastric vagotomy with videotape recordings of barium passage in esophagus, esophageal pressure recordings, and the insulin test. Four of the patients complained of dysphagia after the operation. The dysphagia subsided spontaneously after 1--2 months. Patients with dysphagia showed dilatation of the body of the esophagus and a tapered narrowing in the distal segment. The pressure recordings showed increased frequency and strength of rhythmic pressure waves compared with the preoperative findings. Our results support the theory of a neuromuscular dysfunction.     

Effect of cimetidine on pentagastrin-stimulated gastric secretion before and after proximal gastric vagotomy for duodenal ulcer.

Nine patients with duodenal ulcer were studied before and 2--3 months after proximal gastric vagotomy (PGV). Infustion or cimetidine, 1.2 mg.kg-1h-1, reduced mean gastric acid output, in response to infusion of 1.5 microgram.kg-1h-1 of pentagastrin, by, on an average, 79.4% before and 79.1% after vagotomy. The corresponding values for pepsin output were 66.5% before and 77.0% after the operation. The values were not statistically different. Thus, in terms of per cent inhibition, cimetidine was similarly effective before and after PGV. No correlation was found between per cent reduction of acic output by vagotomy and by cimetidine. The effect of the drug was added to that of the vagotomy. Patients with relapse ulcer after vagotomy are therefore interesting candidates for cimetidine treatment.     

Effect of proximal gastric vagotomy on basal and vagally stimulated gastric bicarbonate secretion in duodenal ulcer patients

Basal gastric bicarbonate secretion and the response to vagal stimulation accomplished by sham feeding were investigated in duodenal ulcer patients before and after proximal gastric vagotomy. Gastric bicarbonate secretion was measured with a computer-based system, which continuously recorded the pH and PCO2 of the gastric perfusate. Preoperatively, basal bicarbonate secretion was 414 +/- 57 mumol/h (mean +/- SEM, n = 9), and the secretory response to vagal stimulation 691 +/- 83 mumol/h (p less than 0.01). About 2 months after proximal gastric vagotomy the basal gastric bicarbonate secretion was 539 +/- 74 mumol/h, and the response to vagal stimulation 693 +/- 72 mumol/h (p less than 0.01). The basal bicarbonate secretion thus increased by 30% after vagotomy (p less than 0.01) but about 1 year later was not significantly different from the basal preoperative value. In the early postoperative period anticholinergics significantly reduced the enhanced basal bicarbonate secretion to a preoperative level. When tested 1 year after the operation anticholinergics did not affect basal bicarbonate secretion but abolished the response to sham feeding. The findings of the study suggest the existence of cholinergic vagal nerve fibres stimulating human gastric bicarbonate secretion and indicate that inhibitory nerve fibres may modulate gastric bicarbonate secretion.     

Fat inhibition of gastric acid secretion in duodenal ulcer patients before and after proximal gastric vagotomy.

In seven duodenal ulcer patients the effect of intraduodenal infusion of 20 ml oleic acid on submaximal gastric acid secretion stimulation by a continuous pentagastrin infusion was evaluated before and after proximal gastric vagotomy. In the control tests 20 ml of saline was given. Before vagotomy, oleic acid evoked a significant inhibition of gastric acid secretion of 25% compared with the controls. This inhibition was abolished after proximal gastric vagotomy. The difference in inhibition before and after vagotomy was significant (P=0.01). It is concluded that the vagus nerve in man plays a decisive role in duodenal fat inhibition of gastric acid secretion.     

Ultrastructure of parietal cells before and after proximal gastric vagotomy in duodenal ulcer patients.

In order to examine whether the reduced acid secretion observed after proximal gastric vagotomy (PGV) is accompanied by intracellular changes in parietal cells, the ultrastructure of parietal cells before and after PGV has been studied in four duodenal ulcer patients. A stereological analysis of electron micrographs shows that after PGV there is a reduction in the volume density of microvilli and the surface density of canalicular membranes. Ten days after PGV there is a temporary increase in the surface density of tubulovesicular membranes. However, 3 months after the operation most of this membrane material has been removed so that the surface density of tubulovesicles at this late stage is only insignificantly higher than before the operation. The relative volume of dense bodies is more than doubled 3 months after PGV, and the observed removal of tubulo-vesicular membranes between the 10 days and the 3 months stage may therefore be due to lysosomal activity.     

Serum group I pepsinogens in unoperated duodenal ulcer patients and in duodenal ulcer patients after proximal gastric vagotomy

Thirty-three duodenal ulcer patients (group A) were examined for gastric acid secretion capacity and serum group I pepsinogens (PG I) under basal conditions. Another group of 36 duodenal ulcer patients (group B), who had undergone proximal gastric vagotomy (PGV) 1 year previously, were similarly examined. Mean basal acid output, mean insulin-stimulated peak acid output, and mean pentagastrin-stimulated peak acid output in the conservatively treated group were 4.5 meq/h, 25.1 meq/h, and 34.4 meq/h, respectively. The corresponding values in the PGV group were 2.5 meq/h, 6.7 meq/h, and 18.5 meq/h. The mean serum PG I concentration in group A was 103.6 ng/ml and in group B 69.9 ng/ml, whereas the mean serum PG I concentration in 34 healthy control subjects was 47.9 ng/ml. The differences in serum PG I concentrations between all three groups were statistically significant (p less than 0.05). An elevated concentration of serum PG I is associated with clinical ulcer disease in unoperated patients, but the wide overlap in the PG I concentration area between duodenal ulcer patients and healthy persons limits the use of PG I determinations in disturbances of gastric acid secretion.     

24-hour intragastric acidity and plasma gastrin after omeprazole treatment and after proximal gastric vagotomy in duodenal ulcer patients

The relationship between suppressed gastric acidity and the increase in plasma gastrin levels after pharmacological and surgical treatment of peptic ulcer disease were compared in this study. Eight patients with chronic duodenal ulcer and referred for proximal gastric vagotomy were studied. 24-hour intragastric acidity and plasma gastrin levels were investigated in the same patients on three consecutive occasions: preentry without any treatment; after 4 weeks of administration of 20 mg of omeprazole daily, and 4-6 months after proximal gastric vagotomy. Intragastric acidity was slightly more reduced by omeprazole (94%) than after proximal gastric vagotomy (78%), with no difference found during the day or night with either. Plasma gastrin levels increased slightly more after proximal gastric vagotomy [284% (median, 2120 pmol.h/L; range, 733-2831 pmol.h/L)] than after omeprazole administration [186% (median, 1586 pmol.h/L; range, 495-2573 pmol.h/L)]. There is strong evidence that the increased plasma gastrin concentration following omeprazole treatment is caused by the reduced intragastric acidity. The slight increase in plasma gastrin concentration following proximal gastric vagotomy despite a lesser reduction in intragastric acidity may be the result of additional effects on gastrin release by the vagotomy. Both treatments resulted in a modest increase in plasma levels of gastrin that were far below the gastrin levels observed in achlorhydric patients, e.g., patients with pernicious anemia.     

A clinical appraisal of the treatment of chronic duodenal ulcer by vagotomy and gastric drainage operation

The authors have followed up 100 patients upon whom a vagotomy plus a drainage operation was performed for chronic duodenal ulceration by one of them (H.C.E.) at King's College Hospital during the 11-year period 1948-1958.     

Alcohol tolerance after proximal gastric vagotomy.

Alcohol tolerance has been studied in 10 patients after proximal gastric vagotomy and six patients after truncal vagotomy and antrectomy. No difference in alcohol tolerance was found before and after proximal gastric vagotomy, while an increased rate of absorption with higher blood levels of alcohol were found after truncal vagotomy and antrectomy.     

Gastric emptying following vagotomy and antrectomy and proximal gastric vagotomy.

Gastric emptying of solid meals labelled with 129Cs was studied in patients for up to one year after vagotomy and antrectomy or after proximal gastric vagotomy. Significant delay was found one month after vagotomy and antrectomy but this had returned to normal by six months. No delay was found after proximal gastric vagotomy. The effect of posture on gastric emptying was also studied in the same subjects. No significant differences were found between gastric emptying in the supine or sitting positions after solid meals.     

Acid secretory response in the late follow-up of proximal gastric vagotomy for duodenal ulcer without Helicobacter pylori eradication

BACKGROUND/AIMS: The profile of acid secretory responses was studied in 20 patients who had had proximal gastric vagotomy (PGV) surgery performed 11-22 years previously in order to treat duodenal ulcers (DU). The presence of Helicobacter pylori was detected in all of the patients. METHODOLOGY: The recurrence of DU was diagnosed in 10 patients and the other 10 remained without recurrence during the follow-up period. The control groups included 10 DU patients with refractory responses to H2 receptor antagonists and 10 "normal" subjects. Both control groups had untreated Helicobacter pylori infection. Measures of 1) basal acid output, 2) acid output for 30 min under continuous i.v. infusion of 0.2 ug/kg/h of pentagastrin acid, and 3) the response for 30 and 60 min after starting a sham feeding, modified by the "chew and spit" technique under simultaneous i.v. infusion of 0.2 ug/kg/h of pentagastrin were performed. Serum gastrin was measured during fasting and at sham feeding. The densities of the gastrin cells of antrum and duodenum were estimated by morphometric counting. RESULTS: Both basal output and acid response to sham feeding plus pentagastrin infusion were higher in the DU controls and DU recurrence patients. The response to pentagastrin infusion did not show any discriminant value. Fasting serum gastrin values increased after PGV, either with or without DU recurrence. Gastrin cell hyperplasia was not demonstrated in any of these groups. CONCLUSIONS: The secretory profile of patients with both late DU recurrence after PGV and Helicobacter pylori infection lies between DU patients refractory to the H2 receptor antagonist approach and those free of DU recurrence after PGV--both of them with current Helicobacter pylori infection. The characteristic pattern of late DU recurrence after PGV and untreated Helicobacter infection is that of increased basal acid output and higher acid secretion responsiveness to sham feeding plus pentagastrin in the presence of higher serum levels of gastrin.