Morphologic and functional evidence of reinnervation of the gastric parietal cell mass after parietal cell vagotomy

The incidence of recurrent ulceration after parietal cell vagotomy varies greatly and the cause is largely unknown. Whether the vagus nerve can regenerate or reinnervate the gastric parietal cell mass after parietal cell vagotomy was investigated. Careful microscopic dissection of the neurovascular bundle in 130 rats allowed the vagus nerve to be divided to the gastric body with preservation of the antropyloric nerve and gastric vasculature. Gastric secretory tests were performed under basal and stimulated conditions after secretagogue and insulin hypoglycemia stimulation.Rats were killed weekly and the vagal nerve distribution examined by electron microscopy. Stimulated gastric acid output decreased from 164 to 26 μmol/hour immediately after operation (p < 0.001). One week after parietal cell vagotomy the nerves were swollen with fibroblast infiltration and collagen around axon groups showed degeneration. By the third week after parietal cell vagotomy, the axons were more densely packed with neurofilaments and acid output had increased to 183 μmol/hour. In the fourth and fifth weeks, the enlarged Schwann cell forum processes had more axons and acid output increased to 262 μmol/hour. By the seventh week, both large and small axons were identified and the acid output was 93 percent higher than the preoperative level (p < 0.001). The sequential neuropathologic changes of vagus nerve degeneration, regeneration and functional reinnervation of the gastric parietal cell mass after parietal cell vagotomy are shown by this study. If this occurs in man, it may be an important cause of recurrent peptic ulceration after parietal cell vagotomy.     

Antral proliferation of G cells after truncal,parietal cell,and antral vagotomy

Antral gastrin cell numbers and serum gastrin levels were studied in five groups of rats: (1) control, (2) truncal vagotomy, (3) truncal vagotomy with pyloroplasty, (4) parietal cell vagotomy, and (5) antral vagotomy. Female Sprague-Dawley rats weighing approximately 225 g were used. Eighteen days after operation radiographic study was performed to assess gastric size and emptying rate. At sacrifice serum was obtained for gastrin assay, gastric pH measured, and the antrum removed for G-cell quantitation. Gastric pH was elevated in all groups except antral vagotomy. Variable degrees of gastric distention and delayed gastric emptying were observed in the rats with truncal vagotomy alone, truncal vagotomy plus pyloroplasty, and antral vagotomy. Parietal cell vagotomy rats had no change in gastric size or emptying rate. Rats with truncal vagotomy, truncal vagotomy plus pyloroplasty, and parietal cell vagotomy had significant increases in serum gastrin levels and in G-cell density. Antral vagotomy resulted in no significant differences from controls. A gastrin inhibitory mechanism residing in the corpus may become inoperative after vagal denervation. Alternatively, proliferation of G cells and increased serum gastrin levels may be a consequence of decreased luminal acid after vagotomy. Vagal innervation of the corpus is a critical variable in control of the antral G-cell mass, but antral innervation is not. Distention by itself does not seem to produce G-cell hyperplasia.     

Effect of parietal cell vagotomy on gastric emptying in duodenal ulcer disease

Gastric emptying was delayed preoperatively in 9 of 19 patients with duodenal ulcer disease, but all 9 patients with evidence of retention by scan were asymptomatic; gastric emptying was normal in the remaining 10 patients. A significant delay in gastric emptying was documented by scan in 17 of 19 patients immediately after parietal cell vagotomy (despite the absence of symptoms of gastric retention). Delayed emptying was demonstrated in three patients who were restudied more than 1 year after parietal cell vagotomy; again these patients had no symptoms of gastric retention at any time. A sustained reduction in basal and stimulated acid secretion in both the early and late postoperative periods was documented in all 19 patients, and serum gastrin levels also remained low. This absence of acid or gastrin stimulation is corroborated by the fact that there was no recurrence of ulcers in these patients during a follow-up period of up to 37 months.     

Antral reactivity: effect of vagal innervation on antral gastrin release by various stimuli

We have demonstrated that temporary vagal blockade does not decrease gastrin release from an isolated antral pouch when gastrin is stimulated by local factors in the pouch. At the same time this sort of temporary vagal blockade decreases the responsiveness of the Heidenhain pouch to endogenous stimuli from the antral pouch but not to exogenous stimuli. These findings suggest that truncal vagotomy may be more efficient and might achieve a greater degree of gastric secretory reduction than does parietal cell vagotomy. The implications of these findings with regard to parietal cell vagotomy in the treatment of duodenal ulcer are discussed.     

A new balanced operation for complex gastroesophageal reflux disease

Twenty-seven patients with advanced gastroesophageal reflux disease have been treated with combined transthoracic parietal cell vagotomy and Collis-Nissen fundoplication. Gastric acid analyses (n = 20) obtained preoperatively and 6 months postoperatively demonstrated a significant late reduction in gastric acid output. Twenty-six patients (96%) have experienced relief of gastroesophageal reflux disease at a mean of 13.3 months (range, 6 to 25 months) without postvagotomy symptoms. Transthoracic parietal cell vagotomy may be considered as an adjunct to mechanical surgical control of advanced gastroesophageal reflux disease.     

Gastric, pancreatic, and biliary secretion and the rate of gastric emptying after parietal cell vagotomy.

We compared the gastric, pancreatic, and biliary secretory responses to a liquid test meal and the rates of gastric emptying of liquid and solid test meals in six patients at least 1 year after parietal cell vagotomy with eight unoperated subjects, one with duodenal ulcer disease and seven normal control subjects. Parietal cell vagotomy decreased gastric acid secretion to one third of normal, but total trypsin and bile salt secretion during the first 150 postcibal minutes were normal. The liquid test meal emptied from the stomach faster after parietal cell vagotomy, the pattern of emptying being exponential in the vagotomy patients and linear in the normal subjects. The rate of gastric emptying of a liquid meal, although faster than normal, was less precipitous after parietal cell vagotomy than after truncal vagotomy plus drainage or subtotal gastrectomy, and trypsin and bile salt concentrations were not diluted to abnormal levels, as occurs after these other procedures. Furthermore, emptying and dispersion of solid food remained normal after parietal cell vagotomy. These findings probably explain, at least in part, the decreased incidence of postprandial dumping and diarrhea that accompanies parietal cell vagotomy compared with the other popular operations for duodenal ulcer.     

Effect of proximal gastric vagotomy and truncal vagotomy and pyloroplasty on gastric functions and growth in puppies after massive small bowel resection.

The effects of truncal vagotomy and pyloroplasty and proximal gastric vagotomy on gastric acid hypersecretion, hypergastrinemia, and growth after massive bowel resection were studied in beagle puppies. In puppies with 80% enterectomy, neither type of vagotomy alters significantly the postprandial hypersecretion of acid from the Heidenhain pouch or the concentration of serum gastrin. Proximal gastric vagotomy tended to decrease the hypersecretion more than did truncal vagotomy. In beagle puppies undergoing 70% small bowel resection, growth was significantly decreased but survival was not impaired. Neither proximal gastric vagotomy nor truncal vagotomy and pyloroplasty reversed completely the impaired growth produced by massive resection. Proximal gastric vagotomy caused a small improvements in growth, while truncal vagotomy and pyloroplasty resulted in a slight decrease in growth. It remains possible that proximal gastric vagotomy could be of value in the management of growing infants with hypersecretion of acid due to short bowel syndrome.     

Proximal gastric vagotomy with carbon dioxide laser: experimental studies in animals

Proximal gastric vagotomy has been widely used as a surgical treatment for peptic ulcer disease. However, it is technically complex and time-consuming. Moreover, it may cause circulatory problems in the gastric mucosa. We have reported a new method of blood flow-preserving vagotomy with a carbon dioxide laser (CO2 laser vagotomy) developed in our laboratory. To assess its efficacy, we used cysteamine-induced ulcer and measured gastric mucosal blood flow in rats. The incidence of cysteamine-induced ulcer formation was reduced significantly in the group that underwent CO2 laser vagotomy compared with a group treated with proximal gastric vagotomy. Gastric mucosal blood flow was significantly better in the CO2 laser vagotomy group. Long-term follow-up of acid reduction was evaluated in dogs by the pentagastrin-stimulation test. Acid reduction in dogs was satisfactory during the 12 months of this study. CO2 laser vagotomy is a new, easy, time-saving, and circulatory-preserving technique for peptic ulcer disease.     

Parietal cell vagotomy in a surgical training program

Parietal cell vagotomy was performed in 48 patients at the Parkland Memorial Hospital and the Dallas Veterans Administration Hospital between April 1977 and January 1981. The maximum follow-up time was 50 months and the average was 28 months. Seventy-five percent of the patients were followed for more than 1 year. There were no operative deaths. Four patients (8.3 percent) had persistent postoperative side effects including two documented ulcer recurrences (4.2 percent). Acid secretion studies were reviewed to characterize the longterm effect of parietal cell vagotomy. These studies demonstrated marked postoperative reductions in gastric acid secretion. The results of this study suggest that with the simplified technique described in this paper, parietal cell vagotomy can be performed with minimal mortality and morbidity by surgical residents under direct staff supervision.     

Decreased parietal cell secretory capacity following vagotomy and pyloroplasty

Although vagotomy reduces acid secretion in vivo, the effects of vagotomy at the level of the parietal cell are not known. In the present study we examined the in vitro secretory characteristics of parietal cells in rabbits 8 weeks following vagotomy compared to unoperated and sham-operated controls. Acid secretion was assessed by the uptake of [14C]aminopyrine (AP) in isolated gastric glands. Also, gastric fundus histology, mucosal thickness, parietal cell density, and gastric gland somatostatin content were examined. Basal AP uptake was decreased following vagotomy (8 +/- 0.4 pmole/mg dry wt) compared to controls (21 +/- 2) (P less than 0.001). Increase in AP uptake by the cholinergic agonist carbachol was unaffected after vagotomy (P greater than 0.5) suggesting intact muscarinic receptors and calcium second messenger system. Increase in AP uptake was significantly reduced following vagotomy by the cyclic AMP-mediated agonist histamine (P less than 0.05) and the cyclic AMP mimetic 8-bromo cyclic AMP (P less than 0.001) suggesting an alteration in the ability of the parietal cell to utilize cAMP following vagotomy. There were no discernible differences in histology, mucosal thickness, or parietal cell number in vagotomized animals compared to controls (P greater than 0.5). There was a significant increase in gastric gland somatostatin content following vagotomy (37 +/- 10 fmole/mg dry wt) compared to control (14 +/- 1.5) (P = 0.025). These results suggest that there is a decrease in the capacity of parietal cells to secrete acid following vagotomy. In addition, the decrease in cAMP utilization following vagotomy suggests that the cAMP second messenger system is dependent, at least in part, on an intact vagus nerve.