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Volume 108, Issue 6
Displaying 1-6 of 6 articles from this issue
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Pharmacological modulation and contribution to mucosal protectionKoji TAKEUCHI1996 Volume 108 Issue 6 Pages 281-293
Published: December 01, 1996
Released on J-STAGE: September 07, 2011
JOURNAL FREE ACCESSBicarbonate secretion from the surface epithelial cells of the gastroduodenal mucosa is an active process depending upon the tissue metabolism and plays an important role as the first line of defense in mucosal protection in collaboration with the mucus gel. This secretion is regulated by humoral and neural factors as well as endogenous prostaglandins (PGs) and is considered to be intracellularly mediated by cyclic AMP in the duodenum and by cyclic GMP in the stomach. Ca2+ also acts as an intracellular mediator in this process. This bicarbonate secretion is markedly increased in response to luminal acid, mediated by PGs and neural factors including capsaicinsensitive sensory nerves, and the impairment of this response is involved in the pathogenesis of various duodenal ulcer models induced by cysteamine, nonsteroidal antiinflammatory drugs and stress. The mechanisms underlying the mucosal protection by HCO3- secretion is two fold; One is the direct neutralization of H+ in the lumen, and the other is the establishment of a pH gradient across the mucus gel aided by the physico-chemical property of the mucus. However, the cellular mechanisms of HCO3- secretion, including the receptors, the mediators and the signal transduction pathway have been poorly understood. The establishment of a method for preparing isolated epithelial cells and the probe for HCO3- secretion in isolated cells is required to further elucidate the mechanism of HCO3- secretion.View full abstractDownload PDF (4067K) -
Kazuo TODOKI, Chang-il LEE, Eiichiro OKABE1996 Volume 108 Issue 6 Pages 295-306
Published: December 01, 1996
Released on J-STAGE: September 07, 2011
JOURNAL FREE ACCESSIn recent years, reactive oxygen species have been implicated in the pathogenesis of a wide variety of disorders. Although the existence of reactive oxygen intermediates in drug metabolism can be inferred from end product analysis or from the effects of antioxidants or enzymes such as superoxide dismutase, only the technique of electron spin resonance (ESR) allows the direct detection of these highly reactive species. However, some free radical species cannot be detected by ESR due to their extremely short half-lives, which result in low steady-state concentrations of the radicals or to short radical relaxation times, which lead to a very broad line. These facts made recent development of spin-trapping and chemiluminescence techniques are widely used to detect free radicals. The goal of this paper is to introduce the various assays available for measurement of reactive oxygen species in biological models. This paper will focus on two topics : (1) the spin-trapping/ESR technique in vitro and vivo and (2) the chemiluminescence-optical biosensor application of this technique, a very sensitive method that has the advantage of being able to provide continuous, online, nondestructive monitoring of reactive oxygen species.View full abstractDownload PDF (3365K) -
Tatsuro YOKOYAMA, Naoki FUJIKURA, Yukinori MASUDA, Ken-ichi SHIKADA, S ...1996 Volume 108 Issue 6 Pages 307-321
Published: December 01, 1996
Released on J-STAGE: September 07, 2011
JOURNAL FREE ACCESSEffects of efonidipine hydrochloride (NZ-105), a dihydropyridine calcium antagonist, on the cardiovascular system were studied in dogs, in which the left anterior descending coronary artery (LAD) was ligated for 50 min. NZ-105 (10 or 30 μg/kg), nifedipine (NIF, 1 or 3μg/kg) or nisoldipine (NIS, 1 or 3μg/kg) was injected i.v. before LAD ligation. NZ-105, NIS or NIF decreased the total peripheral resistance (TPR) and blood pressure (BP) and increased the cardiac output (CO) and regional myocardial blood flow (RBF) dose-dependently. LAD ligation decreased RBF and produced segmental bulging in the ischemic area, decreased BP and CO, and did not change TPR. NZ-105, NIF or NIS attenuated the LAD ligation-induced regional myocardial changes. During LAD ligation, in the presence of NZ-105 (30μg/kg), the values of heart rate (HR), BP, and TPR were lower, and that of CO was higher than those in the absence of the drug. Similar results were obtained with NIS (3μ/kg) except that the value of HR in the presence of NIS was not lower. During ischemia, the presence of NIF (3 μg/kg), did not significantly change the values of the systemic circulation from those observed in the absence of NIF. In conclusion, NZ-105 may exert a cardioprotective effect by decreasing the oxygen demand of the ischemic heart.View full abstractDownload PDF (2305K) -
Izumi MURAKAMI, Shoichi ASANO, Koichi YUKISHIGE, Hideaki NAGAYA, Hiros ...1996 Volume 108 Issue 6 Pages 323-332
Published: December 01, 1996
Released on J-STAGE: September 07, 2011
JOURNAL FREE ACCESSThe effects of lansoprazole given intravenously on indomethacin-induced gastric bleeding and mucosal lesions were investigated in rats in comparison with those of omeprazole, famotidine and ranitidine. Lansoprazole inhibited gastric bleeding induced by indomethacin with an ID50 value of 0.29 mg/kg. Omeprazole and famotidine significantly inhibited gastric bleeding, but ranitidine provided negligible inhibition. A correlation was found between the inhibitory action of lansoprazole on gastric bleeding, and acid secretion, and its inhibitory action on gastric bleeding was almost completely abolished by adding 50 mM-HCl to the gastric perfusate, suggesting that lansoprazole's inhibitory action on gastric bleeding was mainly due to its antisecretory action. Lansoprazole inhibited the development of gastric lesions induced by indomethacin with an ID50 value of 0.10 mg/kg, whereas histamine H2-receptor antagonists did not display a potent inhibitory effect. ID50 values for omeprazole, famotidine and ranitidine were 0.69, 2.58 and 24.6 mg/kg, respectively. These results indicate that lansoprazole has a potent inhibitory action on indomethacin-induced gastric bleeding and mucosal lesions and that it is useful in the treatment of acute gastric mucosal lesions.View full abstractDownload PDF (1174K) -
Nobuhiro INATOMI, Izumi MURAKAMI, Shoichi ASANO, Ikuko INADA, Hiroshi ...1996 Volume 108 Issue 6 Pages 333-343
Published: December 01, 1996
Released on J-STAGE: September 07, 2011
JOURNAL FREE ACCESSThe effects of lansoprazole given intravenously on gastric mucosal lesions, gastric bleeding and acid secretion were investigated in rats in comparison with those of omeprazole, famotidine and ranitidine. Lansoprazole inhibited the formation of gastric mucosal lesions in rats induced by water-immersion stress or aspirin with ID50 values of 0.26 and 0.99 mg/kg, respectively, and also inhibited gastric bleeding induced by hemorrhagic shock or water-immersion stress with ID50 values of 0.46 and 1.22 mg/kg, respectively. Lansoprazole was more potent than omeprazole, famotidine and ranitidine in inhibiting gastric mucosal lesions and hemorrhagic shock- or stressinduced bleeding. Famotidine and ranitidine showed negligible inhibition of water-immersion stress-induced gastric bleeding. Lansoprazole strongly inhibited water-immersion stressstimulated acid secretion in rats, whereas famotidine and ranitidine did not show a potent inhibitory effect. These results indicate that lansoprazole exerts prominent inhibitory actions against the formation of gastric mucosal lesions and gastric bleeding by inhibiting acid secretion, and they show that it is superior to histamine H2-receptor antagonists in inhibiting stress-induced gastric bleeding.View full abstractDownload PDF (1546K) -
1996 Volume 108 Issue 6 Pages a107-a123
Published: December 01, 1996
Released on J-STAGE: September 07, 2011
JOURNAL FREE ACCESSDownload PDF (3519K)
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