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Volume 98 (1991)
- Issue 6 Pages 419-
- Issue 5 Pages 327-
- Issue 4 Pages 245-
- Issue 3 Pages 161-
- Issue 2 Pages 63-
- Issue 1 Pages 1-
Volume 98, Issue 2
Displaying 1-10 of 10 articles from this issue
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Masami SUGIHARA, Kazuo TODOKI, Eiichiro OKABE1991 Volume 98 Issue 2 Pages 63-71
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSThe effect of intravenous injection of 10 μg of a lipopolysaccharide (endotoxin) extracted from E. coli to rabbits on the responses of isolated lingual arteries to des-Arg9-bradykinin (a specific kinins B1-receptor agonist) was studied. Endotoxin injection led to the appearance of the endothelium-independent contractile effect of des-Arg9-bradykinin in the arteries; endotoxin elicited this response when administered at 1, 5 or 20 hr before the experiment, in a time-interval dependent manner. The contractile response to des-Arg9-bradykinin of the arteries isolated from animals receiving endotoxin 20 hr before the experiment was attenuated by des-Arg9-[Leu8]-bradykinin (a specific inhibitor of kinins B1-receptor) or pretreatment of the animals with an inhibitor of protein synthesis (cycloheximide and actinomycin D). When compared with the effect of des-Arg9-bradykinin, bradykinin (a potent kinin B2-receptor, but weak B1-receptor stimulant) caused slight contraction of the arteries; however, this effect was not endotoxindependent and was not modified by des-Arg9-[Leu8]-bradykinin. Effect of in vitro preincubation with endotoxin of the arteries isolated from animals receiving saline 20 hr before the experiment was further studied. The preincubation (for 1 and 5 hr) with endotoxin of the arteries in the presence or absence of plasma had no effect on the sensitivity of the arteries to des-Arg9-bradykinin; the sensitivity was also unaffected in the presence or absence of endotoxin, thus suggesting that there is no interaction between endotoxin and some plasma-related factors with the appearance of the contraction in response to the kinin B1-receptor agonist in the arteries in vitro. Hence, we propose that systemic administration of endotoxin induces the formation of kinin B1-receptors via some cycloheximide or actinomycin D-sensitive steps of protein synthesis in rabbits, and that the activation of kinin B1-receptors by des-Arg9-bradykinin produces contraction of the lingual arteries isolated from the animals treated with endotoxin.View full abstractDownload PDF (7203K) -
Katsuyoshi KAWASHIMA, Kaori KONDOH, Yoshiaki OCHI, Makoto OKA1991 Volume 98 Issue 2 Pages 73-82
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSThe effects of AS-2646 on the acute gastric mucosal lesions induced by various noxious agents and the gastric mucosal defensive factors were studied in rats, and the following results were obtained: 1) AS-2646 (5 ?? 100 mg/kg, p.o.) dose-dependently inhibited the formation of the mucosal lesions induced by ethanol, ethanol-HCl, taurocholate-HCl and serotonin, and its anti-lesion spectrum was the widest among the compounds (cimetidine, pirenzepine, sulpiride and prostaglandin E1) examined here. 2) AS-2646 (5 ?? 10 mg/kg, p.o.) not only improved the changes of gastric mucosal hemodynamics induced by the blood removal and/or the reserpine treatment, but also inhibited the mucosal lesions induced by them. 3) AS-2646 (2 ?? 20 mg/kg, p. o.) antagonized the decrease in the surface gastric mucus and mucosal hexosamine contents induced by stress and/or aspirin. 4) AS-2646 (2 ?? 20 mg/kg, p.o.) caused no significant effect on the gastric mucosal prostaglandin E2 levels. 5) AS-2646 inhibited Campylobacter pylori in vitro. These results indicate that AS-2646 may be useful as a novel antiulcer drug with the defensive factor-potentiating and anti-Campylobacter pylori effects.View full abstractDownload PDF (7842K) -
Yoshiko MASUBUCHI, Toshio KUMAI, Masami TANAKA, Minoru WATANABE, Mari ...1991 Volume 98 Issue 2 Pages 83-90
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSOvariectomy was performed at 4 weeks of age (W), and the rats were used when they were 33 and 75 W old. Systolic blood pressure (BP) was measured by the tail-cuff method. Naloxone (10 mg/kg) was given i.p. Catecholamines (CA) were determined with HPLC. Norepinephrine (NE) was not significantly altered in intact rats by naloxone; however, a significant increase in NE appeared in the plasma, hippocampus, thalamus plus mid-brain and hypothalamus in castrated rats following naloxone. With naloxone treatment, dopamine (DA) was significantly increased in the plasma and hypothalamus, but decreased in the cerebral cortex in intact rats; and with castrated rats, there was a tendency to see an increase in plasma DA and significantly increased levels of DA in the thalamus plus mid-brain and hypothalamus. This suggests that in female brain, lack of estrogen in the castrated rats leads to an increase in intrinsic opiate, and this in turn inhibits CA release. On the other hand, when naloxone was administered to castrated rats, intrinsic opiate was blocked, and, consequently, inhibition of CA release was lost and induction of CA release was enhanced.View full abstractDownload PDF (6428K) -
Terue SUZUKI, Masatoyo KAGOSHIMA, Hideyo SHIMADA1991 Volume 98 Issue 2 Pages 91-98
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSOral administration of HCl (0.2 N, 0.4 N, 0.6 N, 0.8 N) solution produced congestive or hemorrhagic gastric mucosal lesions in rats. Lesion areas were differentiated into two areas (i.e., brown area and black area) macroscopically. Then, fine observations were performed on two areas using a computer image processing system (CIPS) and histological techniques. Cell necrosis from the mucosal surface to the middle mucosal layer were observed in the brown area, and gastric mucosal necrosis that reached to a deeper layer were observed in the black area. These results indicate that histological degree of lesion may be reflected in the macroscopic changes. Concerning the concentration of HCI, over 0.4 N HCl solution induced mucosal lesions, but HCl solution (0.4 N HCl) only produced a brown area. Maximum changes in the mucosal surface were observed at 30 min to 1 hr by 0.6 N HCl and at 15 to 30 min by 0.8 N HCl. Therefore, the best condition for evaluating the preventive effects of anti-ulcer agents is 30 min after treatment by 0.6 N HCl solution and 15-30 min after treatment by 0.8 N HCl solution. These results suggest that this technique may provide both quantitative and qualitative information on histological changes.View full abstractDownload PDF (8496K) -
Masatoyo KAGOSHIMA, Ryuichi HOSHINO, Hideyo SHIMADA1991 Volume 98 Issue 2 Pages 99-111
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSWe have reported the antiulcer activities of a new compound that we named NIK-228 (3-hydroxymethyl-2-methylimidazo (2, 1-b) benzothiazole). In the present report, we studied the antisecretory effects of NIK-228 on basal and stimulated gastric acid secretion using the Congo red sprayed method. Male Wistar rats (200 to 250 g) were used after 24 hr of fasting (without water). NIK-228, atropine and cimetidine were administered orally or intravenously 1 hr before operation for Congo red spraying. NIK-228 (100 mg/kg, p.o.), atropine (5 mg/kg, p.o.) and cimetidine (100 mg/kg, p.o.) all inhibited basal gastric acid secretion. Oral administration of NIK-228 and atropine inhibited gastrin, 2-deoxy-D-glucose (2-DG) and bethanechol-induced acid secretion, but didn't inhibit histamine-induced acid secretion. Cimetidine inhibited all of histamine, gastrin, 2-DG and bethanechol-induced acid secretion. In vagotomized rats, oral and intravenous administration of atropine both inhibited bethanechol-induced acid secretion, but NIK-228 was not inhibited. These results suggested that antisecretory effects of NIK-228 were caused by the central vagal systems.View full abstractDownload PDF (9409K) -
Hisato KAKUSHI, Tsutomu SHIKE, Yoko HAYASAKI, Hitoshi ARITA, Kiyohisa ...1991 Volume 98 Issue 2 Pages 113-120
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSThe effect of (+)-S-145, (1R, 2S, 3S, 4S) (5Z)-7-(3-phenylsulfonylaminobicyclo [2.2.1] hept-2-yl) heptenoic acid on human and guinea pig platelet aggregation was examined. (+)-S-145 sodium salt inhibited human platelet aggregation induced by arachidonic acid (AA), 9, 11-methanoepoxy-PGH2 (U46619), collagen, ADP or epinephrine with the IC50 being 0.047 ?? 0.146 μM in an in vitro system. When (+)-S-145 calcium salt dihydrate was administered orally to guinea pigs, it inhibited AA-, U-46619- or collagen-induced platelet aggregation dose-dependently with the minimum effective dose being 0.03 mg/kg, and the effective duration being maximally 3 hr. The inhibiting potency and effective duration of (+)-S-145 calcium salt dihydrate after multiple administrations, once a day (0.5 mg/kg) for 7 days, were almost the same as those after a single administration. Although (+)-S-145 sodium salt showed a partial agonist effect (shape change) on platelets in vitro, the effect diminished after pretreatment of the platelets with a lower dose of this compound. These data suggest that (+)-S-145 calcium salt dihydrate is an orally effective potent platelet aggregation inhibitor.View full abstractDownload PDF (5643K) -
Tsuyoshi NAGASE, Kei HOTTA, Shigemichi MORITA, Ken SAKAI, Mikio YAMANE ...1991 Volume 98 Issue 2 Pages 121-141
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSThe effects of 1-[2-[bis(4-fluorophenyl)methoxy]ethyl]-4-(3-phenylpropyl) piperazine dihydrochloride (I-893) on the central nervous system were behaviorally and electroencephalographically investigated. Intraperitoneally injected 1-893 (5 ?? 10 mg/kg) dose-dependently increased spontaneous motor activity in mice, but repeated injections did not affect the increase in the locomotor activity. In reserpinized mice, spontaneous motor activity was not increased by oral 1-893. In α-MPT-treated mice, the motor activity was lower than that in vehicle-treated animals with intermediate doses (10 ?? 40 mg/kg, p.o.) of I-893, but there was no difference between the two groups with high doses. In rats with unilaterally 6-OHDA-induced lesion of the nigrostriatal pathway, I-893 induced circling behavior toward the lesioned side. Haloperidol-induced catalepsy in rats was reduced by I-893. Tremorine-induced tremor in mice was inhibited by I-893. The effect was not altered in the mice treated with I-893 for 10 days. Oral I-893 induced stereotypy in rats, but it did not affect methamphetamine-induced stereotypy. Hypnosis induced by barbiturates was antagonized by I-893. In rats treated with I-893 for 6 days, pentobarbital-induced sleep was not different from that in vehicle-treated animals on the day after the final treatment. Intravenous I-893 altered EEGs in the cerebral cortex and amygdala nucleus to low voltage and fast waves and altered hippocampal EEG to theta waves in immobilized rabbits. These results suggest that I-893 inhibits re-uptake of dopamine released by exocytosis and indirectly has dopaminergic effects.View full abstractDownload PDF (16100K) -
Hiroaki MASUNAGA, Reiko TAKAHIRA, Yukuo MURASE, Eisuke Tsuda, Tadanori ...1991 Volume 98 Issue 2 Pages 143-150
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSPharmacokinetics and the time course of pharmacodynamics of recombinant erythropoietin (SNB-5001) were investigated. The plasma concentration of SNB 5001 reached Cmax at 6 ?? 7 hr after the subcutaneous injection and gradually decreased. Most of the SNB-5001 in plasma disappeared at 48 hr. Serum erythropoietin activity changed similarly to plasma SNB-5001 concentration. It was indicated that SNB-5001 moves into the plasma and organs having intact bio-activity after its injection. The decrease in serum iron and increase in unsaturated iron binding capacity (UIBC) began at 8 hr after the injection. Both the trough point of serum iron decrease and the peak point of UIBC increase were 24 hr after the injection. Each value recovered to the initial level at 72 hr. Total iron binding capacity did not change. Increase in reticulocytes began at 24 hr and reached the peak at 72 ?? 96 hr after the injection of SNB-5001. Reticulocytes count recovered to the initial level at 120 hr. The pharmacodynamics time course after the subcutaneous injection of SNB-5001 was the same as that after the intravenous injection. It was indicated that SNB-5001 reached an effective plasma level at the earlier absorption phase after the subcutaneous injection.View full abstractDownload PDF (5750K) -
Hiroaki MASUNAGA, Reiko TAKAHIRA, Tadanori SAWAI1991 Volume 98 Issue 2 Pages 151-160
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSIn order to investigate the clinical usage of SNB-5001 (recombinant human erythropoietin), two types of anemic models induced by drugs were prepared. One group of rats was intravenously injected with 8 mg/kg of cisplatin. These rats temporarily showed leucopenia and thrombocytopenia. Since 2 weeks after the cisplatin injection, rats chronically showed renal failure and moderate anemia. Another group was subcutaneously injected with 15 mg/kg of puromycin, 4 times a week, for 3 weeks. These rats showed hypercholesteremia and hypoalbuminemia, and they showed chronic renal failure and severe progressive anemia. Anemic rats received SNB-5001 (50 or 500 U/kg) once a day for 7 days. In the anemic rats induced by cisplatin, more than 50 U/kg of SNB-5001 dose-dependently increased reticulocytes, red blood cells (RBC), hemoglobin (HGB) and hematocrits (HCT). SNB-5001 apparently improved the anemia induced by cisplatin. On the other hand, in anemic rats induced by puromycin, 50 U/kg of SNB-5001 increased reticulocytes, but did not increase RBC, HGB and HCT. SNB-5001 at the dose of 500 U/kg stopped the progress of anemia in puromycin treated rats. It was suggested that SNB-5001 is useful for the improvement of renal anemia induced by drugs, but the effects are affected by the uremic condition and the stage of renal anemia.View full abstractDownload PDF (7968K) -
[in Japanese]1991 Volume 98 Issue 2 Pages 161-165
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSDownload PDF (5189K)
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