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10. Abstracts of the sixth international conference on experimental ulcer

Author

Aho, P., Lindén, I. -B., Nissinen, E., Pohto, P., Arvidsson, Stefan, Carter, Katharine, Silen, William, Avunduk, C., Polakouski, N. J., Quimby, G. F., Eastwood, G. L., Batzri, Shmuel, Bank, S., Greenberg, R. E., Kranz, V., Ilardl, C., Chemer, J. A., Singh, G., Naik, L., Chiverton, S. G., Hunt, R. H., Dammann, H. G., Kangah, R., Dreyer, M., Müller, P., Simon, B., Ezer, E., Fändriks, L., Jönson, C., Lisander, B., Frydman, G., O'Brien, P., Phelan, D., Flemström, G., Holmes, R., Malcontenti, C., Gompertz, R. H., Man, W. K., Li, S. K., Baron, J. H., Spencer, J., Michalowski, A. S., Gyires, Klara, Kovacs, Aniko, Gutknecht, John, Inauen, W., Rohner, C., Koelz, H. R., Herdmann, J., Schürer-Maly, C. C., Halter, F., Harmon, John, Hakki, Faris, Malthaner, Richard, Saini, Nirmal, Tay, Howard, Japundžić, L., Levi, E., Rakić, Lj., Holzer, P., Lippe, I. Tb., Pabst, H. A., Lorbach, M., Xing, L., Washington, J., Kauffman, G., Kawamura, Takeshi, Koizumi, Fumiaki, Ishimori, Akira, Kivilaakso, E., Kiviluoto, T., Mustonen, H., Konturek, S. J., Brzozowski, T., Dembinski, A., Uarzecha, Z., Konturek, J. W., Bielanski, W., Bogdał, J., Oleksy, J., Krämling, H. -J, Wiesinger, H., Merkle, T., Merkle, R., Enders, G., Drozdowicz, D., Garlicki, J., Kromer, W., Gönne, S., Lam SK, Chen BW, Hul WM, Ng MMT, Cho CH, Luk CT, Ligumsky, M., Sestieri, M., Karmeli, F., Rachmilewitz, D., Evangelista, S., Rovero, P., Mózsik, Gy., Fiegler, M., Garamszegi, M., Jáyor, T., Nagy, L., Sütő, G., Vincze, Á., Odes, HS, Hogan, DL, Ballesteros, MA, Wolosin, JD, Koss, MA, Isenberg, JI, Jávor, T., Vinoze, A., Steinbach, JH, Okabe, S., Kuwahara, Y., Nishida, T., Wang, J. Y., Nagai, H., Takeuchi, K., Palitzsch, K. D., Szabo, S., Pettersson, A., Peitsch, W., Lange, W., Parekh, D., Segal, I., Lawson, H. H., van der Walt, L. A., Sewing, K. -Fr., Beinborn, M., Seidler, U., Jansons, R., Silen, W., Spill, W. F., Pihan, G., Starlinger, H., Schiessel, R., Wenzl, E., Feil, W., Taché, Yvette, Keshavarzian, A., Wibowo, A., Fields, J. Z., Koji-Takeuchi, Nishiwaki, Hideyuki, Okabe, Susumu, Okada, Megumu, Niida, Hiromiti, Takeuchi, Koji, Vantrappen, G., Tarnawski, A., Hollander, D., Krause, W. J., Gergely, H., Yahav, J., Fradkin, A., Diver-Haber, A., Jonas, A., Allen, A., Leonard, A. J., and Pearson, J. P.

Published
1988
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20. Effect of lafutidine, a novel histamine H2-receptor antagonist, on monochloramine-induced gastric lesions in rats: Role of capsaicin-sensitive sensory neurons.

Author

Umeda, Masakazu, Fujita, Akinobu, Nishiwaki, Hideyuki, and Takeuchi, Koji

Subjects
HISTAMINE receptors, SENSORY neurons, THERAPEUTIC use of capsaicin, RATS, GASTROINTESTINAL system, SCIENTIFIC experimentation, CHEMICAL inhibitors
Abstract

AbstractBackground: Lafutidine ((±)-2-(furfurylsulfinyl)-N-(4-(4-(piperidinomethyl)-2-pyridyl)oxy-(Z)-2-butenyl)acetamide) is a novel histamine H2-receptor antagonist and has been shown to exhibit a potent gastroprotective activity in addition to its antisecretory action. In the present study, we examined the effects of lafutidine on the mucosal ulcerogenic and potential difference (PD) responses induced by monochloramine (NH2Cl) in rat stomachs. Methods: Oral administration of NH2Cl at 120 mmol/L produced haemorrhagic lesions in the stomach in unanaesthetized rats. Results: Lafutidine (3–30 mg/kg), given p.o., showed a dose-dependent and significant inhibition against damage caused by NH2Cl: the effect was significant at 10 mg/kg or greater but disappeared almost totally in the sensory deafferented animals following capsaicin pretreatment. Likewise, capsaicin (10 mg/kg, p.o.), but not cimetidine (100 mg/kg, p.o.) exhibited a potent protection against NH2Cl-induced gastric lesions. Topical application of NH2Cl (10 mmol/L) reduced transmucosal PD in ex-vivo stomachs of anaesthetized rats, but this PD response was also prevented by pre-exposure to lafutidine, in a dose-dependent and sensory neuron-sensitive manner. Mucosal exposure to NH4OH (60 mmol/L) also caused PD reduction in ex-vivo stomachs made ischaemic by bleeding from the carotid artery (1 mL/100 g bodyweight), resulting in severe gastric lesions. These ulcerogenic and PD responses caused by NH4OH plus ischaemia were attenuated by prior application of lafutidine as well as taurine, a scavenger of NH2Cl. The former effect was, again, dependent on the sensory neurons. Intraluminal capsaicin but not cimetidine was also effective in preventing a PD response to NH2Cl. Conclusions: These results suggest that lafutidine, but not cimetidine, protects the stomach against NH2Cl, whether occurring endogenously or administered exogenously and that this action may be mediated by capsaicin-sensitive sensory neurons. [ABSTRACT FROM AUTHOR]

Published
1999
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22. Bilateral adrenalectomy worsens gastric mucosal lesions induced by indomethacin in the rat

Author

Takeuchi, Koji, Nishiwaki, Hideyuki, Okada, Megumu, Niida, Hiromichi, and Okabe, Susumu

Abstract

The mechanism by which bilateral adrenalectomy worsens indomethacin-induced gastric lesions was investigated in rats. In sham-operated rats subcutaneously administered indomethacin produced gastric lesions at doses of 10 mg/kg body wt or greater, in association with lowering of blood glucose levels. In a parallel study, indomethacin induced gastric hypermotility at the same dose levels but had no effect on acid output or mucosal blood flow even at 25 mg/kg body wt. Adrenalectomy (2 wk) itself significantly reduced the blood glucose levels (~50%) and markedly potentiated the ulcerogenic and motility responses caused by indomethacin; the ED50values dropped to ~10 times lower than those in sham-operated rats. Both acid output and mucosal blood flow were significantly reduced by adrenalectomy, but these values were increased after indomethacin treatment (3 mg/kg body wt). The ulcerogenic and motility responses caused by indomethacin were significantly reduced by acute infusion of glucose (25% wt/wt, 1.2 ml/h) intravenously in both sham-operated and adrenalectomized rats, and by subcutaneous administration of hydrocortisone acetate (10 mg/kg body wt for 2 wk) in the latter group. When the motility and the ulcer score were determined in the same animals, a highly significant relationship was found between these two factors in both sham-operated and adrenalectomized rats. These results suggest that (a) the increased gastric motility may be a key element in the pathogenesis of indomethacin-induced lesions and in the mechanism for aggravation of the lesions by adrenalectomy, and (b) abrasion of adrenal glands by inducing hypoglycemia may sensitize the system to indomethacin and increase gastric motility.

Published
1989
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23. 16,16-Dimethyl prostaglandin E2aggravates gastric mucosal injury induced by histamine in rats

Author

Takeuchi, Koji, Furukawa, Osamu, Nishiwaki, Hideyuki, and Okabe, Susumu

Abstract

Histamine dihydrochloride (40 or 80 mg/kg, dissolved in 10% gelatin) subcutaneously administered to fasted rats induced few lesions in the gastric mucosa within 4 h. Pretreatment with subcutaneously administered 16,16-dimethyl prostaglandin E2(dmPGE2; ≥10 μg/kg) dose-dependently worsened mucosal injury induced by histamine, mostly with severe hemorrhage in the corpus mucosa along the greater curvature, although dmPGE2alone did not induce any macroscopic damage. The mucosal vascular permeability as measured using Evans blue was slightly but significantly augmented by either dmPGE2(30 μg/kg) or histamine (80 mg/kg) alone, but was markedly increased by histamine in the presence of dmPGE2. The increased vascular permeability occurred within 2 h, and preceded the appearance of hemorrhagic mucosal injury. Both the mucosal injury and the increased vascular permeability caused by histamine (80 mg/kg) in the presence of dmPGE2(30 μg/kg) were significantly reduced by pretreatment with tripelennamine (30 mg/kg) and prednisolone (3 mg/kg), but not affected by atropine sulfate, cimetidine, methysergide, or indomethacin. The stimulation of acid secretion caused by histamine was significantly inhibited by dmPGE2(30 μg/kg). Repeated administration of histamine (40 or 80 mg/kg) in the same area of the stomach in the presence of dmPGE2(30 μg/kg), once or twice daily for 4 days to fed rats, induced more pronounced damage than single-dose treatment. These results suggest that dmPGE2may aggravate gastric mucosal injury induced by histamine in rats, probably due to potentiation of the increased vascular permeability caused by histamine through stimulation of H1-receptors.

Published
1987
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