The purpose of this study was to elucidate the effect of Peptide YY (PYY) on gastric acid output in association with gastric mucosal blood flow (GMBF), acetylcholine (ACh) release in the gastric wall and gastric vascular perfusion pressure in rats. Baclofen stimulated the gastric acid output and GMBF in a dose-dependent manner. Both atropine sulfate and truncal vagotomy completely abolished the effect of balcofen. PYY caused inhibition of baclofen-stimulated gastric acid output and reduction inbaclofen-stimulated GMBF in a dose-dependent manner, however PYY didn't cause inhibition of pentagastrin- and histamine-induced acid output completely. But PYY had no effect on bethanechol-induced acid output. PYY inhibited the [3H] ACh release from cholinergic nerve endings of gastric body evoked by electrial transmural stimulation. PYY had little effect on gastric vascular perfusion pressure in the basal state, and basal gastric acid output. In the present study, it was concluded that the mechanism of the inhibitory effect of PYY on gastric acid output seems to involve reduced ACh release from cholinergic nerves.
In the past 4 years, 11 patients with cardial varix bleeding were experienced. The cardial varices were of 2 types, nodular and serpentine. The nodular varices were caused by gastrorenal shunt and the site of bleeding often existed on the posterior wall. The serpentine cardial varices were an extension of esophageal varices, and the site of bleeding was often on the lesser curvature. The nodular varices had an abundant blood flow. When EIS was performed to these varices independently, the time of contact with the sclerosing agent was so short that no therapeutic effect was obtained. For the purpose of decreasing the blood flow in these varices, TIO was performed first and then EIS was used in the treatment of four cases of nodular varix bleeding. Hemostasis was obtained in two of the four cases with TIO alone, and after the addition of EIS a good hemostatic and varix-reducing effect was noted in all four cases.
The colonic mucosa of 30 patients with ulcerative colitis was analyzed by an immunohistochemical technique. A quantitative evaluation for lymphocyte subsets shows significantly increased numbers of CD3+, CD4+, CD8+, and CD28+ cells in ulcerative colitis cases of histological grades 3, 4 and 5 by Matts' classification comparing to normal control cases. CD4/CD8 ratio in each histological grade of ulcerative colitis was not significantly different from those in normal controls and disease controls (infectious colitis cases). However, CD28/CD3 ratio was increased significantly in ulcerative colitis cases of histological grades 3, 4 and 5 comparing to control cases. Most of the lymphocytes were positive for lymphocyte function-associated antigen-1α (LFA-1α). There were increased numbers of S100-β+ dendritic cells and CD68+ macrophages in the luminal area of the lamina propria. Moreover double stainings revealed that most of the S100-β+ dendritic cells and CD68+ macrophages were intercellular adhesion molecule-1 (ICAM-1, a ligand for LFA-1) positive. These findings suggested that the expression of ICAM1 on S100-β+ dendritic cells and CD68+ macrophages is important by the interaction with T cells and T cell antigen recognition.
A novel monoclonal anti-human coagulation factor XIII (F. XIII) antibody (2C3 antibody) raised in BALB/c mice was established by Kohler and Milstein methods. The monoclonal antibody recognized F. XIII of 85 KD demonstrated by western blotting analysis. Plasma F. XIII-IR levels measured by ELISA with 2C3 antibody were significantly lower in active disease than in quiescent disease in a total of 21 Crohn's disease (CD) patients. Plasma F. XIII levels were significantly lower on admission in CD with fistulas than in CD without fistulas. Relationships between activities of CD and plasma F. XIII levels were shown. No significant relationships, however, were observed between F. XIII-IR levels and nutritional states assessed by TP, ALB, TF, PA, RBP, %IBW. Low levels of F. XIII in active CD patients with fistulas may occur regardless of hyponutrition. By using 2C3 antibody, global functions of F. XIII will become clarified as well as pathologic and diagnostic roles of plasma F. XIII in CD.
We developed an experimental method to measure the gastric and the small bowel transit times in dogs without using X-ray nor radioisotopes. The dog with the ileostomy was given food containing acetaminophen (APAP) and indocyanine green (ICG), then we sampled blood and ileal contents of the dog. We could measure the gastric transit time by detecting plasma APAP and the small bowel transit time by detecting ICG in the intestinal contents. Using this exprimental system, we examined the times after feeding milk or solid meal. The gastric transit time after taking solid meal was longer than that after taking milk, but this difference was not significant, and the small bowel transit time after taking solid meal was significantly shorter than that after taking milk.
Intestinal arterio-venous malformation (AVM) is one of the uncommon cause of gastrointestinal hemorrhage and is usually difficult to diagnose before pathological study. Five operated cases with the AVM were presented. The vascular lesions were studied by barium-gelatine injection and routine histological procedures. The AVM lesion was detected in the proximal jejunum and in the distal ileum in each one case, respectively. In two other cases the AVM lesion was observed as a protruded tortuous vascular plexus in colonic mucosa. By the microangiographical study, it was confirmed that the main lesion of AVM was located in submucosal layer with complicating minute AVM in lamina propria of intestinal mucosa. In the mucosal lesion of AVM it was disclosed that arterization of precapillary arterioles was a remarkable finding. Thickened intimal layer and duplication of internal elastic lamina were recognized in these arteriolar lesions. Two kinds of intestinal AVM were classified, one is located in the submucosal layer and another one is located in mucosal layer. It was suggested that a marked ectasia of mucosal vessels was seemed to be secondary change of the submucosal AVM. The pathogenesis of the mucosal AVM was discussed.
Effects of glucose (225ml, 300kcal) ingestion on hepatic hemodynamics was studied in ten patients with liver cirrhosis and eight patients with non cirrhotic liver disease by per-rectal portal scintigraphy using 99mTcO-4 (direct intramural administration of radioisotope method). Initial portal blood flow index (IP) and collateral index (CI) were calculated from the time activity curve of heart and liver. The value of IP was not significantly changed between before and after glucose ingestion in cases with liver cirrhosis (before: 0.0160±0.0016, after: 0.0204±0.0106). In cases with non cirrhotic liver disease, the value of IP was significantly increased after glucose ingestion (before: 0.0381±0.0145, after: 0.0544±0.0194, p<0.02). These findings suggested increase in portal blood flow via inferior mesenteric vein to the cardiac blood flow. The value of CI before glucose ingestion was significantly increased in cases with liver cirrhosis (0.751±0.156) compared with that in cases with non cirrhotic liver disease (0.517±0.122), but no significant difference in values after glucose ingestion was found between these two groups.
To evaluate prognostic significance of echogenic lesion within small hepatocellular carcinoma (SHCC, _??_2cm in diameter), clinical and pathological findings of 32 cases with SHCC containing echogenic lesion (echogenic SHCC) were compared with those of 55 cases with non-echogenic SHCC. Compared with the non-echogenic SHCC group, the frequency of clinical stage I was significantly higher, and there were significantly more cases with solitary tumor relative to cases with multiple tumors in the echogenic SHCC group. Histologically, the incidence of the HCC composed of well-differentiated tumor cells corresponding to Edmondson's grade I was significantly higher in the echogenic SHCC group than in the non-echogenic SHCC group. Although HCCs tended to become progressively less differentiated with increasing tumor sizes in the both groups, the process of cellular change appeared to proceed more slowly in the echogenic SHCC group. Survival rate after tumor detection was 73% at three years, 56% at five years and 48% at seven years and nine years in the echogenic SHCC group, while it was 46% at three years, 42% at five years and 0% at seven years in the non-echogenic SHCC group. The present results showed that the presence of echogenic lesion within SHCC could be useful prognostic indicator.
We carried out ultrasound guided directpuncture bile aspiration (DPBA) in 58 patients with acute cholecystitis. Symptoms and laboratory findings of acute cholecystitis were rapidly improved after DPBA. NO serious complications were seen during and after the DPBA procedure. It was concluded that DPBA is practical and safe treatment of acute cholecystitis. Furthermore long follow up study revealed that this therapeutic method would be useful and reliable for elder patients and patients with systemic complication.
In the present study, we examined the effect of ursodeoxycholate (UDCA) and it's taurine conjugate (TUDC) on rat pancreatic exocrine secretion using dispersed pancreatic acini (in vitro) and conscious rats (in vivo). In in vitro study 300μM UDCA significantly increased 10-12-10-9 M CCK-8 stimulated amylase release and change of intracellular Ca2+ concentration, but TUDC did not have these effects. In in vivo study intraduodenal infusion of UDCA but not TUDC stimulated pancreatic exocrine secretion. Intravenous infusion of secretin antibody decreased bicarbonate output, however, these increase were not prevented by CCK antagonist. Thus, it was suggested that UDCA has direct action on pancreatic acini and UDCA infused intraduodenally stimulates pancreatic secretion, possibly via the release of a secretin-like substance. The taurine conjugate has weak bioactivity on pancreatic exocrine secretion in both in vitro and in vivo.