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Koji Yakabi

Publications and source records attributed to Koji Yakabi.

10 recordsLinked to original sources
PubMed2006

Histamine mediates the stimulatory action of ghrelin on acid secretion in rat stomach.

Ghrelin, a novel growth hormone-releasing peptide, is present in the rat and human stomach and is known to stimulate acid secretion and stomach motility. However, the mechanism of action of ghrelin is not fully understood. In the present study, we attempted to elucidate the role of histamine in ghrelin-induced acid secretion in rat stomach. Intravenous administration of ghrelin at 0.8 to 20 microg/kg dose dependently increased gastric acid secretion, as measured by the gastric lumen perfusion method. The maximum response was almost equal to that of gastrin (20 microg/kg). These actions were abolished by bilateral subdiaphragmatic vagotomy. Famotidine (0.33 mg/kg) also completely inhibited the effects of ghrelin. Furthermore, ghrelin increased histidine decarboxylase (HDC) messenger RNA (mRNA) levels, as measured by real-time reverse transcription-polymerase chain reaction using LightCycler. The action of ghrelin on HDC mRNA was abolished by vagotomy. Ghrelin did not affect histamine release from isolated vascularly perfused rat stomach. Taken together, these results suggest that ghrelin stimulates gastric acid secretion via a mechanism involving activation of vagal efferent nerve and histamine release from gastric enterochromaffin-like cells.

Animals↗
PubMed2006

Case-control study on the association of upper gastrointestinal bleeding and nonsteroidal anti-inflammatory drugs in Japan.

OBJECTIVE: Studies in Western populations have shown the association of nonsteroidal anti-inflammatory drugs (NSAIDs) and upper gastrointestinal bleeding (UGIB). The role of Helicobacter pylori infection in NSAIDs-related UGIB remains to be studied. We conducted a case-control study in Japan to investigate these related topics. METHODS: Cases of UGIB due to duodenal or gastric ulcer, or gastritis were identified in 14 study hospitals in various areas of Japan. For each case, two controls were identified from population registries in the same district. Information on drugs and other risk factors was obtained from 175 cases and 347 controls by telephone interviews. Anti-H. pylori antibody in the urine was measured in a single laboratory for all the cases and 225 controls. RESULTS: The odds ratio (OR) of UGIB was 5.5 for aspirin and 6.1 for other NSAIDs (NANSAIDs) (p<0.01). The OR for regular use was higher than for occasional use both for aspirin (7.7 vs 2.0) and NANSAIDs (7.3 vs 4.1). Loxoprofen (5.9), frequently used in Japan as a safe 'prodrug', was significantly associated with UGIB. The odds ratio for H. pylori infection was 4.9 and the relative excess risk due to the interaction between H. pylori and the use of NSAID was 1.2 (95% CI: -5.8-8.1). CONCLUSION: NSAIDs including loxoprofen increase the risk of UGIB in Japan as in Western countries, with a similar magnitude of association. There was no evidence of biological interaction between NSAIDs and H. pylori infection.

Adult↗
PubMed2005

Effect of interleukin-8 on histamine release from totally isolated vascularly perfused rat stomach.

BACKGROUND: Recent studies have demonstrated relationships between cytokines and gastric acid secretion. The present study was performed in rats to elucidate the effects of interleukin-8 (IL-8) on gastric acid secretion through an increase in histamine release from the stomach. METHODS: The experiments were performed in gastric lumen-perfused rats for the study of acid secretion and in totally isolated vascularly perfused rat stomach preparations for the study of histamine release. The histamine in the effluent was determined by radioimmunoassay. RESULTS: IL-8 (500 ng) significantly enhanced gastrin-stimulated acid secretion. IL-8, at a concentration of 500 ng/20 ml per 10 min, did not alter basal histamine release, but at 100 ng/20 ml and 500 ng/20 ml it dose-dependently increased gastrin-stimulated histamine release. CONCLUSIONS: IL-8 enhances gastrin-stimulated acid secretion and histamine release from the rat stomach, which may explain the enhancing effect of IL-8 on gastric acid secretion.

Animals↗
PubMed2004

[Arteriosclerosis and gastoduodenal ulcer].

Recent reports suggested an increase in the occurrence of gastroduodenal ulcers in old age people. And it was reported that gastroduodenal ulcers in old age generation has the characteristics which was different from that in young generation. Namiki et al reported that gastric ulcer in old age generation occurs often at the gastric corpus and is larger and deeper and more often with bleeding comparing with that in young people. Furthermore NSAID ulcer is known to occur more often in old age than in young. Although the pathogenesis of the gastroduodenal ulcer in old age is not clear, a decrease in gastric mucosal blood flow with aging might be related that is possibly due to narrowing of arteries based on arteriosclerosis. Since the report by Virchow that suggested the importance of vessels as a cause for gastric ulcer, many studies indicated the involvement of vessels in the pathogenesis of gastroduodenal ulcer. Until recently, however, there were no methods except autopsy to evaluate the severity of arteriosclerosis, therefore the involvement of arteriosclerosis in the pathogenesis was not clarified. Recently a new device that case evaluate the arteriosclerosis by the measuring pulse wave velocity was developed and is now widely used. We undertook to clarify the relation between arteriosclerosis and gastroduodenal ulcer. The result suggested the involvement of arteriosclerosis in the pathogenesis of gastroduodenal ulcer, especially of NSAID ulcer with bleeding. In this manuscript, we refer to the previous reports that suggest the relation between arteriosclerosis and gastroduodenal ulcer.

Aged↗
PubMed2003

Superior mesenteric arterial embolism: treatment by trans-catheter thrombo-aspiration.

A 57-year-old woman with hypertension, mixed mitral valve disease, and atrial fibrillation was admitted to our hospital because of abdominal pain continuing for several hours. On the following day, colonoscopy was performed, and diffuse yellow-white pseudomembranous changes were seen in the right hemicolon, but there were no abnormal findings in the left hemicolon; 24 h after onset, a diagnosis of superior mesenteric arterial embolism was made on the computed tomography (CT) scan findings. Abdominal angiography was performed and showed complete occlusion of the superior mesenteric artery (SMA). Then conservative treatment, using per-catheteric thrombus aspiration, was done, followed by intraarterial injection of tissue type plasminogen activator. After the thrombo-aspiration, the filling deficit of the main artery had disappeared, and the branches on the right side were clearly delineated. After the treatment, the symptoms such as abdominal pain and diarrhea improved accordingly. She was discharged from the hospital 27 days later. Our case suggests that trans-catheter thrombo-aspiration is a possible alternative to open embolectomy for some cases of SMA embolism more than 10 h post-onset.

Catheterization↗
PubMed2003

Neutrophil-derived hydroxyl radicals mediate interleukin-8-induced increases in tetragastrin-stimulated acid secretion in rats.

Until recently, the secretion of gastric acid, which plays an important role in the pathogenesis of peptic ulcer, was thought to be controlled by diet, the autonomic nerves and gut hormones. However, peptic ulcer is now known to be caused by the infection with Helicobacter pylori (H. pylori), so it is possible that inflammation modifies the secretion of gastric acid. We used gastric-lumen-perfused rats to first examine the effect of interleukin-8 (IL-8) on acid secretion and then the involvement of free radicals and neutrophils in the action of IL-8. IL-8 enhanced tetragastrin-stimulated acid secretion and free radical scavengers or inhibitors and the pretreatment with anti-rat neutrophil serum inhibited this effect, which indicates that IL-8 enhances gastrin-stimulated acid secretion and that neutrophil-derived hydroxyl radicals mediate the IL-8-induced increase in acid secretion.

Allopurinol↗
PubMed2002

Neuronal expression of Fos protein in the brain after intravenous injection of gastrin in rats.

The present study examined whether the central neurons are involved in the stimulatory action of gastrin on the secretion of gastric acid. Gastrin (20 microg), which was examined and ascertained to induce a marked increase in gastric acid secretion in gastric-lumen perfused rats, was intravenously injected in Wistar rats under anesthesia with pentobarbital sodium. In the experiments, 1 h after injecting gastrin, rats were perfused and fixed, the brain was removed and sectioned at 40 microm thickness. Every fourth section was treated with anti-c-Fos antiserum, and c-Fos protein was immunohistochemically stained using the avidin-biotin complex method. It was found that c-Fos protein was expressed in neurons of the lateral habenular nucleus, the central nucleus amygdala, the lateral parabrachial nucleus in the pons, and the complex area of the nucleus of the solitary tract and the dorsal motor nucleus of the vagus nerve in the medulla oblongata. The control rats were injected with saline solution, and the brain sections were processed similarly as described above. c-Fos protein was expressed in few neurons in the nuclei above in the control rats. These results suggest that gastrin released into the circulation might stimulate central neurons which, in turn, may relate to the control mechanism for the secretion of gastric acid.

Amygdala↗
PubMed2002

Effects of interleukin-8 and Helicobacter pylori on histamine release from isolated canine gastric mucosal mast cells.

BACKGROUND: In recent studies, the involvement of mast cells in the pathogenesis of Helicobacter pylori infection was suggested. In the present study, using isolated canine gastric mucosal mast cells, we undertook to elucidate the effects of interleukin-8 (IL-8) and H. pylori on histamine release from these cells. METHODS: Enriched canine gastric mucosal mast cells (50% target cells) were incubated in Hanks medium with IL-8, or water extract or sonicate of H. pylori for 15 min at 37 degrees C. The content of histamine in the supernatants and the cell pellets after centrifugation was assayed with a histamine radioimmunoassay (RIA) kit. RESULTS: IL-8 (50 ng/ml) and concanavalin A (20 microg/ml) significantly increased histamine release from enriched gastric mucosal mast cells. Dose-dependent stimulation of histamine release by IL-8 (5-50 ng/ml) was also seen. Water extract and sonicate of H. pylori (10(8) bacteria) increased histamine release from mast cells. A concentration-dependent stimulation of histamine release by water extract or sonicate was also seen. The maximal response of histamine release was seen at the highest concentration of the water extract or sonicate. CONCLUSIONS: The results indicated that IL-8 and H. pylori had stimulatory effects on histamine release from canine gastric mucosal mast cells. The results imply that IL-8 and soluble factors of H. pylori may accelerate inflammation of the gastric mucosa via histamine release from mast cells.

Animals↗