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Studies on the Mechanism for the Gastric Mucosal Protection by Famotidine in Rats

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Studies on the Mechanism for the Gastric Mucosal Protection by Famotidine in Rats Japan. J. Pharmacol. 55, 211-222 (1991) 211 Studies on the Mechanism for the Gastric Mucosal Protection by Famotidine in Rats KeijiMiyata, Takeshi Kamato, Akito Nishida and Kazuo Honda DepartmentofPharmacology, Medicinal Research Laboratories 1, YamanouchiPharmaceutical Co.,Ltd., 21 Miyukigaoka, Tsukuba, Ibaraki 305, Japan ReceivedAugust 10, 1990 AcceptedNovember 15,1990 ABSTRACT-Theeffect of famotidineon gastriclesions induced by the decreasein mucosaldefensive resistance was investigatedin rats and comparedwith those of cimetidine,pirenzepine and cetraxate.Famotidine (0.03, 0.1 and 0.3 mg/kg,p.o.) in- hibiteddose-dependently the developmentof gastriclesions produced by taurocholate- histaminein dosesthat suppressedhistamine-induced acid secretionin pylorus-ligated rats. The H2-antagonistalso prevented gastric mucosal lesions induced by taurocholate-serotonin,iodoacetamide, acidified aspirin and acidifiedethanol. Cimeti- dine, pirenzepineand cetraxateshowed the inhibitoryeffects on almostall types of the gastric lesions,but their inhibitoryeffects were much less potent than those of famotidine.On the other hand, famotidineinhibited the decreasesof gastricmucosal blood flow inducedby acidifiedethanol and the mucosalcontents of glycoprotein in- ducedby waterimmersion restraint stress. In addition,famotidine increased the trans- gastricpotential difference (PD) and promotedthe recoveryof decreasedtransgastric PD induced by acidifiedethanol in rats. These resultssuggest that the preventive effect of famotidineon gastriclesions is attributablenot only to suppression of acid secretionbut to activationof the gastricmucosal defensive mechanisms. Histamine H2-receptor antagonists, famoti- ity. dine, cimetidine and ranitidine, have been Famotidine has been reported to be a po- shown to be effective in preventing the forma- tent H2-receptor antagonist in vitro (10-12) tion of gastric mucosal lesions in rats (1-3) and in vivo (4, 13) with greater antisecretory and in promoting the healing in rat (2, 4) and activity than cimetidine and ranitidine (3, 14, human ulcers (5 -7). The mechanisms by 15). Famotidine has also been reported to in- which H2-receptor antagonists suppress ex- hibit the gastric mucosal lesions that were de- perimental lesions are thought to be secondary pendent on gastric acid (2-4). The aims of to their potent gastric acid antisecretory activ- this investigation were to examine the effect of ity (1, 3). However, cimetidine and ranitidine famotidine on the formation of gastric mucosal blocked acidified aspirin-induced gastric le- lesions induced by the decrease in mucosal de- sions in rats in doses that do not suppress acid fensive factors in comparison with cimetidine, secretion (8, 9), suggesting that mechanisms pirenzepine and cetraxate. other than inhibition of acid secretion might be involved in their mucosal protective activ- MATERIALS AND METHODS caused by acidified (150 mM HCI) aspirin in a dose of 150 mg/kg, i.g., or 60% ethanol, i.g., Materials containing 150 mM HCl (acidified ethanol). Famotidine, cimetidine and pirenzepine One hour after i.g.-administration of acidified hydrochloride were synthesized in our labora- aspirin or acidified ethanol in a 1-ml volume tories. Cetraxate hydrochloride was extracted to rats, the animals were killed by chloroform and purified from Neuer R capsule S (Daiichi and the stomach was removed. The length Pharmaceutical). Each drug was suspended (mm) of each lesion was measured macro- with 0.5% methylcellulose solution and admin- scopically, summed per stomach, and used as istered to rats at a volume of 5 ml/kg. Drugs a lesion index. Drugs were given orally 1 hr used for induction of gastric lesions were before ulcerogens administration. sodium taurocholate (Sigma Chemical), hista- In another series of experiments to evaluate mine dihydrochloride (Wako Pure Chemical), the involvement of endogenous prostaglan- serotonin creatinine sulfate (E. Merck), aspi- dins, indomethacin was subcutaneously in- rin (Sanko Pharmaceutical), indomethacin jected to rats 1 hr before drug administration. (Yamanouchi Pharmaceutical) and iodoaceta- Iodoacetamide-induced gastric lesion: Male mide (Tokyokasei). Taurocholate, histamine Wistar rats weighing 200 to 230 g were used and serotonin, and iodoacetamide were dis- for production of gastric lesions by iodoacet- solved in distilled water, physiological saline amide according to the method of Szabo et al. and tap water, respectively. Aspirin was sus- (16). Briefly, rats were placed in individual pended with 150 mM HCI. Indomethacin was mesh cages to prevent coprophagy with free suspended with physiological saline containing access to food and water. Gastric lesion was 0.2% Tween 80. Other drugs used were tryp- caused by 0.1% iodoacetamide in drinking sin (Sigma Chemical), glucose (Nacalai Tes- water given to rats for 7 days; and on the 8th que) and glucosamine (Sigma Chemical). day, rats were sacrificed by chloroform, and the stomach was removed. The length (mm) Gastric lesion production of each lesion was measured macroscopically, Taurocholate-induced gastric lesion: Male summed per stomach, and used as a lesion in- Wistar rats weighing 200 to 230 g were dep- dex. Test compounds were given orally once rived of food but allowed free access to water daily to rats during the 7 days. for 24 hr before the experiments. Acute gas- tric lesions were induced by taurocholate Gastric acid secretion alone and in the combination with histamine Male Wistar rats weighing 200 to 230 g were or serotonin. Just after 30 mM taurocholate deprived of food, but allowed free access to was given intragastrically in a 1-ml volume, tap water for 24 hr before the experiments. histamine was injected i.p. in a dose of 100 With the rats under ether anesthesia, the mg/kg or serotonin was injected sub- abdomen was incised, and the pylorus was li- cutaneously in a dose of 20 mg/kg. Four hours gated. They were placed in individual mesh later, the animals were killed by chloroform, cages to prevent coprophagy. Four hours lat- and the stomach was removed. The area er, the animals were killed by chloroform, (mm2) of each lesion was measured macro- and the gastric contents were analyzed for scopically, summed per stomach, and used as volume and acidity. Acidity of the gastric juice a lesion index. Drugs were given orally 1 hr was determined by titration with 0.05 N before taurocholate administration. NaOH using an automatic titrator (Hiranuma, Aspirin or ethanol-induced gastric lesion: Comtite-7) to an endpoint pH of 7.0. In Male Sprague-Dawley rats weighing 210 to 230 another series of experiments to examine the g were deprived of food and water for 24 hr influence of histamine against gastric secretion before the experiments. Gastric lesions were in pylorus-ligated rats, histamine at a dose of 100 mg/kg was intraperitoneally injected to was exposed, and two catheters were passed the rats immediately after the abdomen was into the stomach through an incision in the sutured. Test compounds were given orally 1 duodenum and were held in place by a liga- hr before pylorus ligation. ture around the pylorus. One catheter, which was filled with 4% agar in saturated KCI, Measurement of gastric mucosal blood flow served as the intragastric electrode. The circuit Male Sprague-Dawley rats weighing 200 to for the PD recording was coupled with an in- 240 g were deprived of food with free access different electrode placed in the abdominal to water for 24 hr before the experiments. cavity filled with saline. Both the intragastric Under urethane (1.25 g/kg, i.p.) anesthesia, and intraperitoneal electrodes were placed in the trachea was cannulated and the abdomen separate beakers containing saturated KCl was opened. The esophagus was ligated with- solution in which a balanced Ag-AgCI elec- out disturbing the vagus nerves. Gastric trode was positioned. The changes in PD were mucosal blood flow was measured using a la- continuously monitored using a recorder ser Doppler blood flowmeter (TSI, Laserflo; (Rikadenki, R-52) connected to the millivolto- BPM403) according to the method of Saita et meter (Toa Electronics, HM-16S). The second al. (17). The optical flow probe was inserted gastric catheter led to a pH glass electrode of into the stomach through a temporary gastric the flow type (Toa Electronics, GS-80) to de- fistula, which was prepared using a termine the changes in pH of fluids emerging polyethylene tube, in the forestomach and was from the pylorus and which was connected to placed on the gastric mucosa. The probe was a pH meter (Toa Electronics, HM-16S) for mounted in a commercially available balancer simultaneous measurement of the changes in (Physio-Tech). Approximately 30 min after PD. The whole interior of the stomach anesthesia, 60% ethanol containing 150 mM was gently rinsed with warmed saline 3 to HCl in a 1-m] volume was intragastrically 4 times, and then 3 ml of saline was instilled administered through a gastric fistula. The into the stomach. The perfusion of warmed changes in gastric mucosal blood flow was saline (2 ml/min) was controlled by a peristal- continuously monitored. Drugs were given tic pump (Taitec, N-18) located at the middle orally 30 min before urethane anesthesia. of entry or exit tube connected to the fistula or to the pH glass electrode. Measurement of the transgastric potential dif- Approximately 30 min after anesthesia, the ference (PD) perfusion system was interrupted, and the The experimental procedure was essentially solution in the stomach was withdrawn. The the same as that described by Takeuchi and stomach was then exposed for 10 min to 3 ml Okabe (18). Male Sprague-Dawley rats of acidified ethanol. After acidified ethanol weighing 200 to 250 g were derived of food for exposure, the stomach was gently rinsed again 24 hr but water was allowed ad libitum. After several times, another 3 ml of saline was instil- anesthesia with urethane (1.25 g/kg, i.p.), the led, and the perfusion system was resumed. trachea of the rat was cannulated. The abdo- Drugs were given orally 30 min before men was opened and the stomach was ex- urethane anesthesia.
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