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PURPOSE: Ischemic colitis develops after a sudden decrease in colonic blood supply and has a variety of clinical manifestations. The aim of this study was to assess the role of platelet activating factor in the pathogenesis of ischemic colitis with use of the platelet activating factor antagonist TCV-309. METHODS: Rats were randomly divided into four groups. Rats in Group RV underwent ring attachment around the rectum to induce partial obstruction and ligation of the marginal vessels of the left colon. As control, rats in Group R underwent the ring attachment and rats in Group V underwent the vascular ligation. Rat in Group C underwent sham operation. The effects of TCV-309 on lesion formation in the colon were evaluated. Thiobarbituric acid reactant level was determined in colonic mucosa, and the incidence and severity of ischemic lesions were also determined. RESULTS: Lesions of colitis were frequently observed in Group RV. TCV-309 did not prevent lesion formation, nor did it suppress the increase in thiobarbituric acid reactant level in Group RV. However, TCV-309 mitigated the severity of the lesion. CONCLUSIONS: Partial obstruction of the colon tends to induce ischemic colitis, and additional ischemia completes lesion formation. Platelet activating factor may play a role in the progression of ischemic lesions.

Patients with "reflux" gastritis after gastrectomy suffer from a variety of symptoms, and this type of gastritis may sometimes compromise the quality of life of these patients. Since Helicobacter pylori is considered to be one of the most important pathogenetic factors in gastritis, the association between H. pylori and reflux gastritis was investigated in this study. A total of 145 patients with gastrectomy were entered into the study. Five biopsy specimens from the gastric remnant were taken at upper gastrointestinal endoscopy. One specimen was examined pathohistologically, and the remaining four were examined for H. pylori infection. Fifty-two patients (36%) demonstrated H. pylori infection. The prevalence of H. pylori was significantly higher in patients who had a partial gastrectomy, and it was significantly lower in patients who had undergone gastrectomy more than 4 years previously. The histologic gastritis score in patients with H. pylori infection was significantly higher. Furthermore, H. pylori was eradicated in patients with some symptoms of gastritis and no bile reflux to the residual stomach at endoscopy; in these patients the symptoms were relieved and the histologic gastritis score decreased significantly. In conclusion, possible involvement of H. pylori is suspected in the pathogenesis of "nonreflux" gastritis after gastrectomy.

In this report, we briefly present the case of a 67-year-old woman who developed recurrent glucagonoma with lymph node metastasis. An immunohistochemical study of the metastatic tumor revealed immunoreactivity of glucagon and protein kinase C (PKC)-alpha, -beta, and -gamma in the tumor cells, two types of which were seen by electron microscopy. One type had abundant secretory granules and mitochondria, while the other had few granules and mitochondria. Some granules were similar to typical A cell granules and others were atypical. An immunoelectron microscopic demonstration revealed PKC-alpha, -beta, and -gamma immunostaining in the cytoplasm of all the tumor cells, while some secretory granules had PKC immunostaining, and others had no immunostaining. Thus, it appears that metastatic glucagonoma and its associated granules are composed of two types of mature and immature cells or granules. As immunoreactivity of PKC-alpha and -gamma was found in the tumor cells, but not in the normal A cells of the islets of Langerhans, the PKC subspecies alpha and gamma, which are not present in normal pancreatic A cells, may exist in human glucagonoma cells.

A case of adult Bochdalek hernia with gastric volvulus in a naturally healthy 54-year-old man is described. The patient was seen at the hospital because of epigastralgia, appetite loss and weight loss for 6 months. He was diagnosed as Bochdalek hernia with gastric volvulus by chest X-ray photographs, contrast radiography of the upper gastrointestine and thoracic CT scans. At laparotomy the stomach was rotated around its mesenteric axis and the antrum was dislocated into the thorax through the left posterior-lateral diaphragm defect. His symptoms disappeared after the operation. Adult Bochdalek hernia with gastric volvulus is very rare and only 5 cases including this case have been reported in this country. In the case of adult Bochdalek hernia with gastric volvulus, definitive operation should be selected even if the patients is asymptomatic.

The influence of 16,16-dimethyl prostaglandin E2 (16,16-dm PGE2; an agent used for the prevention of stress ulcer after hepatectomy of the cirrhotic liver) on liver regeneration after hepatectomy was studied in rats. The following results were obtained. Ulceration after the stress of 6 h of water immersion was markedly suppressed in rats treated with 30 r/kg of 16,16-dmPGE2 as compared with the untreated controls. In animals that received hepatectomy alone, the gastric pH and gastric mucosal blood flow showed significant reduction from the preoperative levels. In animals that received hepatectomy plus 16,16-dmPGE2 treatment the postoperative reduction in the gastric pH and gastric mucosal blood flow was suppressed, suggesting the effectiveness of 16,16-dmPGE2 treatment in the prevention of stress ulcer after hepatectomy of the cirrhotic liver. The 3H-thymidine uptake percentage and thymidine activity 24 h after hepatectomy and the DNA content 30 h after hepatectomy were significantly higher in animals treated with 16,16-dmPGE2 than in the untreated controls. In animals that were treated intraperitoneally with 50 mg/kg of indomethacin 6 h before hepatectomy the mitotic index 30 h after hepatectomy was markedly lower than that in untreated controls. This indomethacin-induced reduction in the mitotic index tended to be normalized by treatment with 16,16-dmPGE2. These results suggest that 16,16-dmPGE2 treatment effectively prevents stress ulcer and favorably affects hepatic regeneration after hepatectomy of the cirrhotic liver.

We investigated the response of gastric vessels to prostaglandin (PG) E2 after intra-duodenal release of bile in rats with obstructive jaundice. The animals were divided into four groups according to duration of bile duct obstruction (BDO): control and 1 week (W), 2W, and 3W groups. Prolonged BDO decreased gastric mucosal blood flow (BF) significantly. The BF recovered after the release of BDO in the 1W and 2W groups, but not in the 3W group. BDO decreased PGE2 content in gastric mucosa in the 1W, 2W, and 3W groups. PGE2 decreased vascular perfusion pressure of the isolated stomach in the control and 2W groups, but not in the 3W group. The response of gastric vessels to PGE2 was poor in the 3W group compared with the control and 2W groups. Decreased PGE2 in the gastric mucosa and decreased response of gastric vessels to PGE2 may affect gastric blood flow in obstructive jaundice.

There is disagreement with regard to the involvement of dopamine (DA) receptors in gastric motility. The mechanisms of the inhibitory effect of DA on rat gastric motility was investigated in association with acetylcholine (Ach) release in the present study.In vivo vagotomized, splanchnicectomized rats and control rats were used, and gastric movement was determined as the gastric motility index after DA administration. In vitro study of Ach release from the circular muscle strips of the gastric corpus was investigated after administration of domperidone, SCH23390, phentolamine, or propranolol.In the in vivo study DA inhibited gastric motility in a dose-dependent manner. Vagotomy and splanchnicectomy had no effect on the inhibitory effect of DA. In vitro study DA inhibited [3H]-Ach release in a dose-dependent manner. The inhibitory effect of DA was antagonized by domperidone but not by phentolamine, propranolol, or SCH23390.Inhibition of gastric motility by dopamine is independent of extrinsic innervation and seems to be mediated by DA2 receptors in the gastric wall.

Recent studies have shown the presence of dopamine (DA) in gastric and duodenal mucosa, and changes in gastric mucosal DA content have been observed in patient with acute ulcers. Immunohistochemical demonstration of the distribution of DA in gastric mucosa under stress was studied by light and electron microscopy. In the control group, DA was present in the gastric gland proper in the gastric corpus and antrum on light microscopy, and on the surface of mucous granules in chief cells, mucous neck cells, and surface epithelium on electron microscopy. In the stress group, DA in gastric mucosa was almost undetectable on light and electron microscopy. Further, in this group serum DA concentration was significantly higher in the portal vein than in the abdominal aorta. Endogenous DA in gastric mucosal cells may affect gastric mucosa differently from exogenous DA, and stress may release endogenous intracellular DA into extracellular spaces.

The inhibitory mechanism of dopamine (DA) on rat gastric motility was investigated in association with DA receptors. Gastric movement was assessed according to the method of Jacoby et al and was expressed with the system of Ludwick et al. (1968). DA inhibited gastric movement in both the corpus and antrum in a dose-dependent manner. Domperidone, a specific antagonist of DA2 receptor, suppressed DA-induced inhibition of gastric movement in a dose-dependent manner. SCH23390, a specific antagonist of DA1 receptor did not affect DA-induced inhibition of gastric movement. LY171555, a specific agonist of DA2 receptor, inhibited gastric movement in both the corpus and antrum in a dose-dependent manner. SKF38393, a specific agonist of DA1 receptor, did not affect gastric movement. These results indicate that DA plays an important role in the inhibitory regulation of gastric motility, through DA2 receptor but not DA1 receptor.

The results of treatment of eight cases of ulcerative colitis and five cases of Crohn disease experienced in our department were investigated. Five of the eight cases of ulcerative colitis achieved remission by conservative treatment alone, and the mean proportion of relapse into the active stage of the lesion, reckoned in months after discharge was 32%. As for surgical cases, total colorectectomy-ileostomy, subtotal colectomy-anastomosis of the ascending colon and rectum and the Kock method were respectively performed in each case. On the other hand, two of the five cases of Crohn disease showed postoperative relapse. In one case presenting relapse in the duodenum and pyloristenosis, gastrectomy (the Billroth II method) was performed and another case achieved remission using Salazopyrin. Many cases of ulcerative colitis are benign and are found in juveniles, necessitating the positive consideration of the conservative method of spontaneous anus. With regard to the surgery for Crohn disease, the cause of relapse is unknown, and there have also been cases of relapse reported from microlesions so small that they are impossible to diagnose during surgery. It may therefore be necessary to deal cautiously with excision of a skip lesion in which there is no complication or en bloc excision of each lymph node.

We experimentally studied the influence of vagotomy on hepatic regeneration in rats after hepatectomy of cirrhotic livers. In animals that underwent hepatectomy plus vagotomy the reduction in gastric pH was suppressed, but gastric mucosal blood flow was less than that in control animals that received hepatectomy alone. The suppression of 3H-thymidine uptake percentage and thymidine kinase activity after hepatectomy was more marked in animals treated with hepatectomy plus vagotomy than in controls treated with hepatectomy alone. Hepatic DNA level tended to be lower in animals treated with hepatectomy plus vagotomy than in controls. In animals treated with hepatectomy plus vagotomy, the peak level of the mitotic index was lower and the hepatic regeneration rate was evidently suppressed. These results suggest that it is not appropriate to apply vagotomy, during hepatectomy of cirrhotic livers, for the prevention of postoperative stress ulcer because it causes a marked reduction in gastric mucosal blood flow and suppresses hepatic regeneration.

Changes of noradrenaline (NA) and prostaglandin (PG) E2 in gastric mucosa and gastric wall blood flow (GWBF) were investigated after stress load in rats with obstructive jaundice. We found that water immersion and restraint stress more easily increased the ulcer index and decreased GWBF, corresponding to a decrease of the NA and PGE2 contents in the gastric mucosa, as the duration of jaundice increased. Administration of PGE2 reduced the increase of the ulcer index and the decrease of the GWBF and NA contents in the gastric mucosa. It is suspected that the rapid decrease of NA and PGE2 is connected with the rapid decrease of GWBF after stress load in obstructive jaundice, and we reached the hypothesis that both PGE2 and NA mutually regulate local GWBF.

Until now, 21 cases of Crohn's disease (78% of total cases of this disease) have been surgically treated at our department. Of thse cases, 14 received a curative surgery (complete resection of the lesion). We analyzed postoperative relapes of the disease in these 14 cases. Postoperative relapse was seen in 2 (50%) of the 4 patients with Crohn's disease of the small bowel and 3 (33%) of the 9 patients with Crohn's disease of the small and large bowels. Of these 5 cases of postoperative relapse, 4 had relapse at a site close to the anastomoses. The mean timespan from the surgery to the relapse was 3 years and 3 months in patients with Crohn's disease of the small bowel and 11 months in those with Crohn's disease of the small and large bowels. The relapse rate was 13% for the patients with a preoperative IOIBD (International Organization for the Study of Inflammatory Bowel Disease) score of 4 or less and 67% for those with a preoperative IOIBD score of 5 or more. Of the 9 cases in whom the unaffected intestine was resected for 10 cm more proximal (adoral) from the lesion, no one showed postoperative relaps. Of the 5 cases in whom the unaffected intestine was reseacted for less than 10 cm proximal from the lesion, all showed postoperative relapse. However, no correlation was found between the relapse rate and the length of the resected unaffected intestine distal (towards the anus) from the lesion. Reoperation was done in 2 cases because of fistulation.