In spite of numerous reports of secondary lactose intolerance in post-gastrectomy, only a few reports have been found regarding changes of sucrose absorption after resection of gastrointestinal tract. Since the sucrose is contained more in quantity than the lactose in ordinary adult food and the fructose, one of the component of sucrose, is the non-active transported monosaccharide in the intestine, the sucrose absorption after resection of the gastrointestinal tract would reveal one of the most important changes of the intestinal function. In this paper the author studied the oral tolerance test of sucrose (STT) and glucosefructose (GFTT) and intestinal sucrase activity in dogs with gastrectomy or massive small bowel resection. The following results were obtained. 1) The sucrase activity of the upper small intestine was depressed to about 75% of the preoperative status in gastrectomized dogs with Billroth I. 2) The intestinal sucrase activity of the oral portion and anal portion at anastomotic site corresponded to each activity of the preoperative upper small intestine and lower small intestine, revealing no compensatory changes of sucarse activity of the remnant of the small intestine in dogs with massive small bowel resection. So, the dogs with massive small bowel resection showed the absolute intestinal sucrase deficiency as a whole on account of loss of resected bowel activity. 3) In spite of elevated fructose absorption curve in both STT and GFTT, the decreased fructose absorption ratio estimated from STT and GFTT fructose curve showed the relative sucrose intolerance in gastrectomized dogs. 4) In addition to depressed fructose absorption curve in both STT and GFTT the decreased fructose absorption ratio revealed not only absolute sucrose intolerance but also relative intolerance in dogs with massive small bowel resection. Therefore, the dogs with gastrectomy or massive small bowel resection became of sucrase deficiency with each characteristic pattern, leaving the different sucrose intolerance in both gastrectomy or massive small bowel resection each other.
The common causes of common bile duct dilatations are choledocholithiasis, histology of operative procedure of biliary system and chronic pancreatitis etc, but we have had six cases of common duct dilatations without any of the above changes for the past 3 years; these changes are usually recognized as primary benign papillary stenosis. In all six cases, parapapillary diverticula were found at the second portion of duodenum by hypotonic duodenography. All cases had been confirmed to having no bile duct stones at operation except one case who had a small gall bladder stone. The width of their common bile ducts were 10-20mm. The pathological changes of our cases were various; such as; one case of opening orifice of the papilla of Vater at the inner wall of diverticulum, two cases of severe fibrosis of papilla (papillitis chronica fibrosa), one case of bending of the lower part of common duct pressured by diverticulum and of papillary insufficiency, one case of multiple diverticula and one case of abscess of gallbladder with papillary stenosis. Relation between primary papillary lesion and parapapillary diverticulum seemed to be apparent in our six cases.
In 10 control rats and 9 rats with common bile duct obstruction, histological studies weredone on the pancreas and the parotid gland. Amylase was measured in these tissues andserum. The following results were obtained. 1. After common bile duct obstruction, the parotid gland showed almost normal histologicalfindings. 2. Amylase content of the parotid gland was normal after common bile duct obstruction. 3. Serum amylase was decreased after common bile duct obstruction. 4. In mild changes of the pancreas, the parotid gland showed no histological or functionalchanges. These results would rule out histological or functional influence of common bile ductobstruction on the parotid gland.
In our preceding studies, it was reported that experimentally produced acute pancreatitiscaused atrophic and degenerative changes of parotid gland. In the present study, the lightand electron microscopic examinations were performed in order to comfirm these findingscytologically. In the pancreas, many pathological findings of acute pancreatitis were found after ligationof common bile duct. In the parotid glands, general cytological changes were not markedcompared with pancreas, but in 96 hours after ligation of common bile duct, several cytologicalchanges were identified as follows 1) decrease of secretory granules in the acinar cells 2) dilationand vacuolation of granular endplasmic reticulum 3) spare appearence of lipid droplets. Among these findings, the appearence of lipid droplets were not caused by pancreatitis.Because in another experiment of ligation of common bile duct at liver hilar portion, manylipid droplets were observed in acinar cells of pancreas and parotid glands.
Each 20 normal men and women were examined for pepsin activities by the modified Anson's method, and comparison was made between those after stimulation with histalog and tetragastrin. Electron-microscopic studies were also made with the chief cells before and after stimulation. The concentrations of pepsin after stimulation by histalog or tetragastrin reached the peak value in 10 to 20minutes after the stimulation, gradually decreased thereafter and reverted to the control level on 120minutes after the stimulation. Pepsin output reached also to the peak value in 10 to 20minutes after the stimulation. There was no statistical difference between the effects of histalog and of tetragastrin on the pepsin outputs, although the former appeared to be slightly stronger than the latter and the time of the maximum pepsin output was reached slightly earlier by the tetragastrin than by histalog. After 20 minutes of stimulation, fusion of zymogen granules in the cytoplasm of the chief cells was increased and electron density of the granules was decreased. Cytoplasmic membrane, confronting the lumen, became irregular in shape and the buddings of the zymogen granules or the secreting processes of zymogen into the lumen were frequently observed.
The effect of calcium on gastric secretion was studied in 18 peptic ulcer patients and acase of suspected Z-E syndrome obtained from our inpatient service. After 2hour infusion of normal saline solution, Calcium Gluconate containing 15mg/kgof calcium ion was administered intravenously with the saline at the rate of 5.3ml/min. overthe following 4hours. The blood and gastric juice samples were collected every hour during6hours. In each collected sample of gastric juice acidity and peptic activity were measuered, and in each blood sample serum gastrin level and immunoreactive insulin were assayed bythe radioimmunological method. The value of serum calcium level was 4.48±0.06mEq/l before calcium infusion, andit rised to 5.73±0.37EEq/l at the 4th hour after calcium infusion was begun. The pepticactivity, acidity, secretory volume and serum gastrin level increased as the serum calcium levelrised, however serum insulin did not increased. In peptic ulcer patients the average of basal acid output was 2.75±0.75mEq/h. andcalcium stimulated acid output was 4.80±0.90mEq/h. The latter was equal to 2.22±0.31times of the former. One hour calcium stimulated acid output was 37±8% of gastrinstimulated MAO in peptic ulcer patients, and it was 78% in Z-E syndrome case. The acid secretory ability of calcium was inferior to gastrin, to the contrary its pepticsecretory ability was superior to gastrin. The authors discussed the mechanism of gastric secretory ability of calcium and speculatedthat calcium might stimulate gastric secretion through gastrin release.