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Volume 46 (1988)
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Volume 46, Issue 1
Displaying 1-15 of 15 articles from this issue
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Masakatsu TAKAHASHI, Yoshiki DEGUCHI, Hiroshi KANETO1988 Volume 46 Issue 1 Pages 1-5
Published: 1988
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSStudies have been carried out to determine how the analgesic effect of morphine and the development of tolerance to the effect would be influenced by concurrent exposure to stresses in mice. Application of footshock (FS) stress, which produces analgesia mediated by opioid μ-receptors, or psychological (PSY) stress, which produces analgesia in a manner more closely related to opioid κ-receptors, did not affect the analgesic effect of morphine, but completely blocked the development of tolerance during 5 daily concomitant treatments. On the other hand, forced swimming (SW) stress induced analgesia (SIA), which was not antagonized by naloxone, suppressed morphine analgesia, but failed to block the tolerance development. The blockade of the development of tolerance to morphine analgesia by stresses may not be attributed to the analgesic effect induced by the stresses because a combination of weak FS stress, which induces no analgesia, also effectively suppressed the development of morphine tolerance. In addition to the opioid mechanism, an adrenergic mechanism can not be excluded because of the reserpine antagonism of these SIAs.View full abstractDownload PDF (259K) -
Hitoshi KONTANI, Yoichi KAWABATA, Ryozo KOSHIURA1988 Volume 46 Issue 1 Pages 7-15
Published: 1988
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSWe studied the effects of baclofen on the bladder contraction induced by infusion of Tyrode's solution into the urinary bladder in anesthetized rats. Baclofen (5 mg/kg, i.v.) completely inhibited bladder contraction and abolished the efferent discharges recorded from the left pelvic nerve, causing the bladder pressure to rise until solution leaked from the penis. The inhibitory effect of baclofen (5 mg/kg, i.v.) could not be reversed by picrotoxin (1 mg/kg, i.v., twice with an interval of 10 min) or naloxone (1 mg/kg, i.v.). In parallel with convulsion, strychnine (1 mg/kg, i.v.) contracted the bladder which had been inhibited by baclofen and generated electrical activities consisting of efferent discharges and electromyograms. The dose of intracerebroventricularly or intrathecally injected baclofen which completely inhibited the bladder contraction was 0.1 or 10 μg, respectively. After the inhibition of bladder contraction by i.v. injection of baclofen, electrical stimulation of the sacral cord could contract the bladder and cause a fall in bladder pressure to around the level existing after micturition. From these results, the active site of baclofen which is related to the inhibition of bladder contraction is thought to be the micturition center in the brain stem.View full abstractDownload PDF (505K) -
Yoh-ichi KUREBAYASHI, Takuya IKEDA, Yasuaki OSADA1988 Volume 46 Issue 1 Pages 17-25
Published: 1988
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSThe protective effect of cetraxate, an antiulcer and antigastritis agent, on HCl·ethanol-induced gastric lesions was investigated in rats. Oral administration of 1 ml of HCl·ethanol (60% ethanol in 150 mM HCI) induced within 1 hr linear hemorrhagic necrosis in the gastric mucosa. Either oral or intraperitoneal treatment with cetraxate (30-300 mg/kg) significantly inhibited such macroscopic gastric lesions in a dose-related manner, and the inhibition at the oral highest dose (300 mg/kg) was practically complete. Histological analysis also confirmed that cetraxate effectively prevented deep mucosal necrosis, but showed that it was without protective effect on the surface epithelial disruption and submucosal edema in response to HCl·ethanol. The antilesion activity of cetraxate was of statistically significance for at least 3 hr after a single injection, and it was hardly affected by the removal of the gastric contents just prior to application of the necrotizing agent. However, subcutaneous treatment of rats with indomethacin (5 mg/kg) resulted in a partial but significant attenuation in the protection afforded by cetraxate, suggesting that dual mechanisms related and unrelated to endogenous prostaglandins may be involved in its protective activity. The results demonstrate that cetraxate is a potent cytoprotective agent effectively preventing the formation of gastric mucosal necrosis induced by HCl·ethanol.View full abstractDownload PDF (857K) -
Hiroshi AZUMA, Kiyoe MIZUSHIMA-KASAHARA, Satomi SEKIZAKI, Masayuki ISH ...1988 Volume 46 Issue 1 Pages 27-33
Published: 1988
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSAdenosine produced a slight but concentration-dependent relaxation in rabbit aortic strips preconstricted with norepinephrine. The effect of adenosine was markedly augmented in the presence of hydralazine. On the other hand, the adenosine-induced relaxation was attenuated by 8-phenyltheophylline, but was unaffected by indomethacin, nordihydroguaiaretic acid and quinacrine, indicating that adenosine acts via purinergic receptors and that vasodilating metabolites of arachidonic acid are not involved in the relaxation. The adenosine-induced relaxation remained unaffected by S-(p-nitrobenzyl)-6-thioguanosine (NBTG) or 2'-deoxycoformycin (2'DCF), alone or combined. NBTG significantly inhibited the incorporation of [3H] adenosine, while the content of [3H] compound was increased by 2'DCF, but was unchanged by hydralazine. Hydralazine also augmented the 2-chloroadenosine-induced relaxation. These results suggest that the augmentation of adenosine-induced relaxation with hydralazine does not result from an inhibition of adenosine transport and/or adenosine deaminase. When adenosine was added, relaxation was elicited with concomitant increase in cAMP, but with no significant change in cGMP. In the presence of hydralazine, the cAMP increasing effect of adenosine was augmented, and the level of cGMP increased with adenosine. These changes in cyclic nucleotide levels might at least in part explain the augmentation of adenosine-induced relaxation with hydralazine.View full abstractDownload PDF (438K) -
Heitaroh IWATA, Chuzo IWATA, Toshio MATSUDA1988 Volume 46 Issue 1 Pages 35-42
Published: 1988
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSThe difference in functional SH groups between two isozymes (α(+) and α forms) of (Na++K+)-ATPase was examined using omeprazole, a hydrophobic drug which was reported to modify SH groups of gastric (H++K+)-ATPase. Omeprazole inhibited rat brain and kidney (Na++K+)-ATPase activities in a time- and dose-dependent manner, and it inhibited incorporation of [3H]NEM into the catalytic subunit of the enzymes. The inhibition was greater in the brain enzyme than in the kidney enzyme. The inhibition of the brain enzyme showed a lag time, whereas the kidney enzyme was inhibited according to pseudo-first order kinetics. The inhibition by omeprazole of Na+-dependent phosphorylation and K+-stimulated phosphatase activity in the brain enzyme preparation was parallel with that of the overall (Na++K+)-ATPase reaction, while the partial reactions of the kidney enzyme showed different sensitivities to inhibition by omeprazole. Furthermore, the inhibition by omeprazole of [3H]NEM reactivity in the brain α(+) form was greater in the presence of SDS than in the absence, whereas the inhibition in the brain and kidney α forms was less in the presence of SDS than in the absence. These findings suggest that the isozymes of (Na++K+)-ATPase differ in hydrophobicity of SH groups of their catalytic subunits.View full abstractDownload PDF (446K) -
Hidetada KOMATSU, Masami KOJIMA, Naoyuki TSUTSUMI, Shuichiro HAMANO, H ...1988 Volume 46 Issue 1 Pages 43-51
Published: 1988
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSWe investigated the mechanism of inhibitory action of tranilast on chemical mediator release by antigen-antibody reactions. Tranilast (10-5-10-3 M) inhibited antigen (DNP-Ascaris)-induced histamine release from sensitized purified rat mast cells (PMC), but did not show an obvious influence on intracellular cyclic AMP. 45Ca uptake into PMC induced by antigen (300 μg/ml) was obviously suppressed by tranilast (10-6-10-3 M). Tranilast (10-4 M) inhibited antigeninduced histamine release from and 45Ca uptake into PMC independently of the presence or absence of glucose in the medium. On the other hand, 2-deoxyglucose (10-2 M) markedly inhibited both responses in the absence but not in the presence of glucose. Tranilast slightly inhibited Ca-induced contraction of guinea pig taenia coli, but had no influence on aggregation of rabbit platelets. Verapamil (10-6-10-4 M) had no effect on antigen-induced histamine release, but it markedly suppressed Ca-induced contraction and platelet aggregation. From these results, we suggest that the mechanism of inhibitory action of tranilast on the release of antigen-induced chemical mediator from mast cells involves the suppression of Ca uptake, but that its mode of action is apparently different from those of 2-deoxyglucose and verapamil.View full abstractDownload PDF (476K) -
Hidetada KOMATSU, Masami KOJIMA, Naoyuki TSUTSUMI, Shuichiro HAMANO, H ...1988 Volume 46 Issue 1 Pages 53-60
Published: 1988
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSWe investigated the mechanism of inhibitory action of tranilast, one of the anti-allergic drugs, on the release of slow reacting substance of anaphylaxis (SRS-A). lonophore A23187 (0.5 or 0.2 μg/ml)-induced SRS-A release from rat peritoneal exudate cells (PEC) or human leucocytes was inhibited by tranilast (10-5-10-3 M). The IC50 (the concentration which gives 50% inhibition) of tranilast on these reactions was approx. 10-4 M. Prostaglandin (PG)E2 release from sensitized purified rat mast cells (PMC) by a specific antigen (DNP-Ascaris) was markedly suppressed by tranilast (10-3 M). Similarly, ionophore A23187-induced PGE2 and 6-keto-PGF1α releases from rat PEC were inhibited by tranilast (10-5-10-3 M). DNP-Ascaris antigen-induced 3H-arachidonic acid (AA), 3H-PGE2, 3H-PGF2α and 3H-PGD2 releases from rat PMC were markedly suppressed by tranilast (10-5-10-5 M), DSCG (10-5-10-4 M) and mepacrine (10-3 M). The activity of AA-converting enzymes such as 5-lipoxygenase, cyclooxygenase, PGI2 synthetase, and glutathione-S-transferase was hardly influenced by tranilast (10-5-10-3 M). From these results, we suggest that the mechanism of the inhibitory action of tranilast on the release of SRS-A is related to the processes prior to dissociation of AA from the membrane phospholipids.View full abstractDownload PDF (420K) -
Masahiro TOHKIN, Naomi YOSHIMATSU, Takashi MATSUBARA1988 Volume 46 Issue 1 Pages 61-69
Published: 1988
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSThe effects of epinephrine and dinitrophenol (DNP) on Ca2+-fluxes and energy metabolism were compared in isolated rat hepatocytes and perfused rat livers. Epinephrine increased the cytosolic free Ca2+ concentration ([Ca2+]i), with Ca2+ being extruded into the extracellular space. DNP also increased [Ca2+]i, but did not cause Ca2+ extrusion into the extracellular space. The maximal change of [Ca2+]i caused by DNP was much larger than that by epinephrine. In the absence of extracellular Ca2+, the transient increase of [Ca2+]i due to epinephrine declined rapidly, while the DNP-induced increase was not affected. Although increased oxygen consumption was detected after the addition of epinephrine or DNP, tissue ATP contents decreased markedly by DNP, but not by epinephrine, suggesting that the Ca2+ extrusion is energy-dependent. DNP could activate glycogenolysis even after the depletion of the epinephrine-responsive Ca2+ store in isolated perfused liver, indicating that this intracellular Ca2+ store differed from the DNP-responsive store.View full abstractDownload PDF (477K) -
Kiyohisa UCHIDA, Hisato KAKUSHI, Tsutomu SHIKE1988 Volume 46 Issue 1 Pages 71-77
Published: 1988
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSLatamoxef, 1-S replaced and/or decarboxylated derivatives of latamoxef were examined for their effects on ADP-, collagen- and platelet activating factor (PAF)-induced rabbit platelet aggregation in vitro. The results were compared with those of cefotaxime, cefmetazole, carbenicillin and aspirin. Latamoxef produced a dose-dependent inhibition of platelet aggregation at concentrations over about 4 mM, and the potency was almost similar to that produced by the other β-lactam antibiotics, although the inhibiting effect on ADP-induced aggregation was more potent for latamoxef, whereas that on collagen-induced aggregation was stronger for cefmetazole and carbenicillin. The inhibitory effect of β-lactam antibiotics on collagen-induced aggregation was, however, much weaker than that of aspirin. With respect to drug potency, replacement of the oxygen atom in the oxacephem ring with a sulfur atom caused no significant change in ADP-induced aggregation or slightly stronger inhibition of collagen- and PAF-induced aggregations. The decarboxylated derivatives of latamoxef and the 1-S replaced analogue of latamoxef showed slightly weaker inhibition of ADP-induced aggregation, but much stronger inhibition of collagen- and PAF-induced aggregation than the parent compounds. These data suggest that 1) the oxygen atom in the oxacephem ring is not responsible for the inhibitory effect of latamoxef on platelet aggregation and 2) the carboxyl group in the amide side chain had no significant role in this inhibition.View full abstractDownload PDF (352K) -
Einosuke TANAKA, Koichi NAKAMURA, Shogo MISAWA, Yukio KUROIWA1988 Volume 46 Issue 1 Pages 79-82
Published: 1988
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSPretreatment of male and female rats with cimetidine decreased the amount of 3-hydroxymethylantipyrine in the 24-hr urine, but urinary antipyrine and 4-hydroxyantipyrine were increased compared to that of the corresponding control rats. On the other hand, the amount of norantipyrine and the total amount of antipyrine and its metabolites were not changed by cimetidine, ranitidine and famotidine. These data suggest that ranitidine and famotidine have little effect on the microsomal mixed function oxidase system in male and female rats.View full abstractDownload PDF (213K) -
Masafumi INOUE, Keijoh HIFUMI, Kazuyoshi KURAHASHI, Motohatsu FUJIWARA1988 Volume 46 Issue 1 Pages 83-85
Published: 1988
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSEffects of uptake2 inhibition by corticosterone on tyramine-induced noradrenaline (NA) overflow under control, glucose-deprivation, anoxia and anoxia with glucose-deprivation were examined in perfused rat heart. Uptake2 inhibition by corticosterone (100 μM) had no effect on the NA overflow under control and glucose-deprivation, but significantly augmented the NA overflow by about 40% and 25% under anoxia and anoxia with glucose-deprivation, respectively. These results indicate that the uptake2 mechanism is at least in part responsible for the inactivation of NA under anoxic conditions in the perfused rat heart.View full abstractDownload PDF (161K) -
Shinichi KURAKATA, Masaharu FUKAMI, Kouichi KITAMURA1988 Volume 46 Issue 1 Pages 86-89
Published: 1988
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSOral treatment of female NZB/NZW F1 hybrid mice with captopril prevented the development of proteinuria and prolonged survival in mice demonstrating slight (trace to 1+) proteinuria. Captopril treatment also markedly reduced the incidence and magnitude of proteinuria and prevented death in mice showing significant (3+ or greater) proteinuria. Histopathological studies of the kidneys of treated mice further demonstrated improvements in the renal lesions of autoimmune mice. The mechanisms whereby captopril treatment influences the course of disease in NZB/NZW mice are not known.View full abstractDownload PDF (238K) -
Munekazu GEMBA, Nobuyuki FUKUISHI, Sachiko NAKANO1988 Volume 46 Issue 1 Pages 90-92
Published: 1988
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSTwo days after cisplatin was injected into rats, urinary N-acetyl-β-D-glucosaminidase (NAG) and γ-glutamyltranspeptidase (γ-GTP) activities increased. The urinary excretion of NAG continued to rise until 4 days after the injection of cisplatin, the last day examined. However, the increase in urinary γ-GTP excretion which lasted for 2 days returned to its control level 4 days after cisplatin injection. The alkaline phosphatase activity in urine was unaffected by cisplatin injections. The antioxidant N-N'-diphenyl-p-phenylenediamine attenuated these increases in enzyme activities caused by cisplatin. The results of this study suggest that monitoring the change in urinary activities of some enzymes is the method of choice for detecting cisplatin nephrotoxicity and that the increase may involve the generation of free radicals by cisplatin.View full abstractDownload PDF (176K) -
Ikuko KIMURA, Tetsuo MATSUI, Masayasu KIMURA1988 Volume 46 Issue 1 Pages 93-96
Published: 1988
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSBasal pulse rate (PR) and systolic blood pressure (BP) in the tail artery of diabetic KK-CAy mice were compared with those of alloxan- or streptozotocin (STZ)-induced diabetic ddY mice. Significantly higher PR and BP were obtained by the above three kinds of diabetic states when compared with the pre-diabetic state (KK-CAy) or the non-diabetic state (ddY mice). The PR and BP alteration in diabetic KK-CAy mice were significantly different from the PR one in alloxanmice and from the BP one in STZ-mice, respectively. Both increases in PR and BP by the diabetic state suggest an anticholinergic state.View full abstractDownload PDF (187K) -
Terutake NAKAGAWA, Sigeru KURASAKI, Tiharu MASUDA, Kiyoharu UKAI, Sato ...1988 Volume 46 Issue 1 Pages 97-100
Published: 1988
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSThe role of dopaminergic and cholinergic functions in the genesis of an electroretinogram is unclear. The present study was carried out to elucidate the direct actions of some psychotropic drugs in isolated rabbit retinas. Methamphetamine and apomorphine decreased dose-dependently the b-wave amplitude at a dose of 10-7-10-5 g/ml. On the other hand, chlorpromazine and haloperidol, as well as atropine and amitriptyline, increased dose-dependently the b-wave amplitude at the same dose range. These data support the idea that dopaminergic and cholinergic systems play an important role in the genesis of the ERG.View full abstractDownload PDF (206K)
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