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Volume 59 (1992)
- Issue 4 Pages 427-
- Issue 3 Pages 267-
- Issue 2 Pages 137-
- Issue 1 Pages 1-
Volume 59, Issue 3
Displaying 1-22 of 22 articles from this issue
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Mikio Ito, Daisuke Shii, Tetsuya Segami, Ryoji Kojima, Yoshio Suzuki1992 Volume 59 Issue 3 Pages 267-274
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSZ-103 at 1 to 25 mg/kg, p.o. prevented 100% ethanol-induced gastric mucosal lesions in a dose-dependent manner. Z-103 at 3 to 25 mg/kg, p.o. significantly elevated gastric mucosal super-oxide dismutase (SOD)-like activity 1 hr after its administration to normal rats. In addition, Z-103 at doses (10 and 25 mg/kg, p.o.) which prevented 100% ethanol-induced gastric lesion further increased gastric mucosal SOD-like and glutathione peroxidase (GSH-px) activities elevated by 60% ethanol. Z-103 (10 and 25 mg/kg) significantly inhibited the increase in thiobarbituric acid-reactive substances in gastric mucosa injured by 60% ethanol. The combination with cycloheximide, a protein synthesis inhibitor, completely abolished the prevention of 60% ethanol-induced gastric mucosal lesions and the elevation of both free radical scavenging enzyme activities in the mucosa by Z-103 (10 mg/kg, p.o.). These results suggest that Z-103 may partly protect rat gastric mucosa against ethanol-induced damage by scavenging oxygen-derived free radicals via increases in the synthesis of SOD-like and GSH-px enzymes in the mucosa.View full abstractDownload PDF (559K) -
Susumu Okabe, Keiko Takagi, Hideki Igata, Shinichi Kato, Kenichi Shimo ...1992 Volume 59 Issue 3 Pages 275-289
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSWe examined the effects of a new compound, N-[3-[3-(piperidinomethyl)phenoxy]-propyl]-2-(2-hydroxyethyl-l-thio)acetamido·2-(4-hydroxy benzoyl)benzoate (Z-300), on the histamine H2-receptor, gastric secretion in rats and dogs, and acute gastro-duodenal lesions or chronic gastric ulcers in rats. Roxatidine acetate hydrochloride (roxatidine), a known histamine H2-receptor antagonist, was used as a reference compound. The pA2 values for Z-300 and roxatidine for the isolated guinea pig atrium were 6.8 and 7.0, respectively. These agents at <10-5 M did not affect the contraction of guinea pig ileum in response to carbachol. Z-300, administered either orally or parenterally, significantly inhibited the basal and histamine-stimulated gastric acid secretion in rats. Gastric acid secretion stimulated by histamine, pentagastrin or carbachol in Heidenhain pouch dogs was also significantly inhibited by the compound. The effect persisted for <7 hr in the case of histamine-stimulation. Oral Z-300 significantly protected the gastric mucosa from water-immersion stress-, indomethacin-, aspirin- and HCl·ethanol-induced lesions and protected the duodenal mucosa against mepirizole- and cysteamine-induced ulcers. These effects on gastric secretion and lesion formation were, as a whole, stronger than those observed with roxatidine. Z-300, but not roxatidine, significantly accelerated the spontaneous healing of acetic acid ulcers induced in rats and prevented the delay in ulcer healing caused by indomethacin. The mechanism of action of Z-300 on acute lesions and chronic ulcers appears to be mostly related to its potent antisecretory and mucosal-protective activities.View full abstractDownload PDF (793K) -
Toshio Yamagishi, Teruyuki Yanagisawa, Norio Taira1992 Volume 59 Issue 3 Pages 291-299
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSThe fura-2 microscopic fluorimetric method was used to examine the effects of the thromboxane A2 analogue, U46619, on the force of contraction and intracellular calcium concentrations ([Ca2+]i) in canine coronary arteries. Upon cumulative application, U46619 increased [Ca2+]i and force. Depolarization by 20 mM KCl potentiated the increase in [Ca2+]i and increased the maximum force induced by U46619. In 5 mM KCl-PSS, the reduction of resting [Ca2+]i by cromakalim (3 × 10-6 M) was greater than that by verapamil (3 × 10-6 M). Cromakalim and verapamil inhibited the increases in [Ca2+]i and force induced by U46619 in 5 mM KCl-PSS. In 90 mM KCl-PSS in the presence of U46619, verapamil inhibited the increases in [Ca2+]i and force, whereas cromakalim did not inhibit them at all. The inhibitory effect of cromakalim was counteracted by depolarization by 20 or 25 mM KCl. Curves in the presence of U46619 which related force to [Ca2+]i were shifted to the left compared with that in the absence of U46619, suggesting that U46619 increases the Ca2+-sensitivity of the contractile proteins. Thus, U46619 produces Ca2+ influx through L-type Ca2+ channels, which are deactivated by hyperpolarization induced by cromakalim.View full abstractDownload PDF (550K) -
Issei Takayanagi, Koji Shiraishi, Noriko Kokubu1992 Volume 59 Issue 3 Pages 301-305
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSRabbit isolated iris dilator strips were contracted by norepinephrine, an α1A- and α1B-nonselective agonist, but not by methoxamine, an α1A-selective agonist. The concentration-response curve for norepinephrine was considerably inhibited by chloroethylclonidine. The pA2 values for WB4101 and 5-methylurapidil were 8.16 ± 0.09 and 7.84 ± 0.08 (means ± S.E. of 8-12 experiments), respectively, and significantly smaller than the values reported in the rat renal artery and thoracic aorta, and rabbit bronchus, where the α1A-subtype is predominant. These results suggest that the rabbit iris dilator contains primarily the α1B-subtype. Clonidine and tizanidine did not contract the rabbit iris dilator but shifted the curve for norepinephrine in a parallel manner, suggesting that they interact with the α1B-subtype and act as competitive antagonists in this muscle. Methoxamine (up to 10-3 M) had no effect on the contractile response to norepinephrine, suggesting that methoxamine does not interact with the α1B-subtype.View full abstractDownload PDF (333K) -
Kiyoshi Mizuguchi, Takashi Yano, Masahiro Kojima, Yasuo Tanaka, Masaak ...1992 Volume 59 Issue 3 Pages 307-312
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSWe examined the effect of ethyl all-cis-5, 8, 11, 14, 17-icosapentaenoate (EPA-E) with high purity on circulating lipids in rats under several experimental conditions. In normolipidemic rats, EPA-E decreased the lipids in a dose-dependent manner. Clofibrate (100 mg/kg/day) was more potent in lowering the lipids than EPA-E (1000 mg/kg/day). In high cholesterol diet-fed rats, EPA-E (300 mg/kg/day) decreased the total cholesterol. However, clofibrate (300 mg/kg/day) had little effect on the total cholesterol. In hypertriglycemic rats induced by corn oil, EPA-E (300 mg/kg/day) or clofibrate (100 mg/kg/day) reduced the rise of triglycerides. EPA-E (300 mg/kg/day), clinofibrate (100 mg/kg/day) or clofibrate (300 mg/kg/day) caused a significant reduction in the lipids induced by the injection of Triton WR-1339. Furthermore, EPA-E (300 mg/kg/day) or clinofibrate (100 mg/kg/day) decreased the elevation of lipids produced by feeding the rats a casein-rich diet. These results show that EPA-E possesses potent inhibitory activity on experimental hyperlipidemia induced either exogenously or endogenously.View full abstractDownload PDF (428K) -
Yoshihiro Nakata, Hiroyuki Takamatsu, Naoyoshi Kuroyanagi, Hiroaki Nis ...1992 Volume 59 Issue 3 Pages 313-319
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSSubstance P (SP) binding protein of rat brain was solubilized by digitonin. The solubilized proteins were then purified by sequential gel filtration, concanavalin A lectin Sepharose, and SP-affinity chromatography. The calculated molecular weight of this purified SP binding protein was 76-74 kDa on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The rabbits were immunized with the purified protein and resulting polyclonal anti-sera were tested. The immune serum significantly inhibited [3H]SP binding to the 3-[(3-cholamidopropyl)dimethylammonio]-1-propane sulfonate solubilized membrane fractions from rat brain, whereas pre-bleed antiserum failed to inhibit the binding. This polyclonal antibody also inhibited the activity of 45Ca influx into astroglioma cells stimulated by SP, but does not inhibit that stimulated by histamine. Furthermore, this polyclonal antibody recognized the 76-74 kDa band as assessed by Western blotting. These data strongly suggest that this polyclonal antibody could recognize a part of the natural SP receptor site.View full abstractDownload PDF (629K) -
Hiromu Kawasaki, Shigeru Nakamura, Koichiro Takasaki1992 Volume 59 Issue 3 Pages 321-331
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSPressor responses to intracerebroventricular (i.c.v.) injection of clonidine were investigated in conscious spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). Clonidine (1-10 μg, i.c.v.) caused a dose-dependent pressor response and decrease in heart rate in both SHR and WKY. In SHR, low doses (1, 2.5 μg) but not high doses (5, 10 μg) of i.c.v.-clonidine induced a depressor response following the pressor response. Both pressor and depressor responses to i.c.v.-clonidine were significantly greater in SHR than in WKY. In both SHR and WKY, pressor responses to i.c.v.-clonidine were abolished by pentobarbital anesthesia, pretreatment with i.v.-furosemide (5 mg/kg), 24-hr water deprivation and pretreatment with i.c.v.-yohimbine (100 μg), but not by pretreatment with i.v.-yohimbine (100 μg) and i.c.v.-prazosin (10 μg). On the 1st day after surgery for arterial catheter implantation, SHR reduced their water intake, and i.c.v.-clonidine (5 μg) caused a slight pressor response, whereas the same dose of clonidine on the 7th day after surgery resulted in a marked pressor response. These results suggest that clonidine caused a central α2-adrenoceptor-mediated pressor response, which is greater in SHR than in WKY and is sensitive to body fluid volume changes and anesthesia.View full abstractDownload PDF (624K) -
Yoshitaka Nishimura, Hachiro Usui, Aritomo Suzuki, Noriyoshi Kajimoto, ...1992 Volume 59 Issue 3 Pages 333-338
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSThe relaxant effects of calcitonin gene-related peptide (CGRP) and other drugs were compared in basilar artery rings obtained from stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto rats (WKY). In addition, the relaxant effect of CGRP on basilar arteries from spontaneously hypertensive rats (SHR) was examined. Relaxation induced by CGRP was independent of the presence of endothelium, and it was markedly increased in SHRSP when compared to WKY. In contrast, acetylcholine-induced relaxation was endothelium-dependent and did not differ between the two groups. Enhanced CGRP-induced relaxation was also found in SHR when compared to WKY. However, the relaxant response was greater in SHRSP than in SHR. No significant differences were found in the relaxation induced by isoproterenol, forskolin, dibutyryl cyclic AMP, and 3-isobutyl-1-methylxanthine in endothelium-rubbed arteries of WKY and SHRSP. These results suggest that CGRP produces endothelium-independent relaxation in the rat basilar artery, and that the enhanced CGRP-induced relaxation found in SHRSP may not be associated with alterations of vasodilation mediated by cyclic AMP.View full abstractDownload PDF (368K) -
Satomi Kitagawa, Yu Yamaguchi, Masaru Kunitomo, Noriko Imaizumi, Motoh ...1992 Volume 59 Issue 3 Pages 339-347
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSThe present investigation was undertaken to characterize the relaxing responsiveness in aortic strips from rats with arteriosclerosis, which was produced by excess vitamin D2 (VD) administration followed by treatment with or without a high-cholesterol diet for 6 weeks (VD + CHOL and VD group, respectively). This arteriosclerotic aorta was characterized by medial calcification and intimal cell proliferation. Helical strips of thoracic aorta were suspended in oxygenated Krebs-Henseleit solution. Under precontraction with noradrenaline, endothelium-dependent relaxations to acetylcholine were significantly attenuated in the VD and VD + CHOL as compared with the control. Relaxation to calcium ionophore A23187 was also significantly attenuated in the VD + CHOL. However, the relaxing responses to acetylcholine and A23187 in aortas from rats fed a high-cholesterol diet alone remained unaffected. Nitroglycerine caused an equal degree of relaxation in aortas from control and arteriosclerotic rats. There was a significant negative correlation between the relaxing response to acetylcholine and the calcium content in the aorta. These results indicate that in arteriosclerotic rat aortas, the endothelium-dependent relaxation to acetylcholine is impaired in proportion to the degree of calcification, and such impairment is facilitated by cholesterol feeding but can not be attributed to hypercholesterolemia or vascular cholesterol deposition.View full abstractDownload PDF (1141K) -
Hisanori Takanashi, Michitaka Akima1992 Volume 59 Issue 3 Pages 349-355
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSThe purpose of the present study was to investigate the relationship between the effects of 15(R)-15-methylprostaglandin E2 (arbaprostil) on gastric blood flow (GBF) and its protective effects on gastric lesions in rats. The GBF of anesthetized rats was measured by two different methods: Total blood flow into the stomach (total GBF) was determined by means of an ultrasonic pulsed Doppler flow meter; and gastric mucosal blood flow (mucosal GBF) was measured by nonradioactive microspheres. Systemic blood pressure (SBP), heart rate (HR) and gastric vascular resistance (GVR) were recorded simultaneously. Arbaprostil (10-100 μg/kg) given i.v. did not affect resting total or mucosal GBF even though it decreased SBP and GVR. Significant improvement of the total and mucosal GBF decreased by indomethacin pretreatment (10 mg/kg, i.v.) was observed by administration of arbaprostil (10-100 μg/kg, i.v.) in a dose-dependent manner. Furthermore, i.v.-administration of this agent, in the same dose-range, prevented the formation of gastric lesions induced by indomethacin. The present result suggests that mitigation for the ischemic state of the gastric mucosa may be one of the important mechanisms for the prophylactic and curative effect of arbaprostil on gastric lesions induced by indomethacin.View full abstractDownload PDF (502K) -
Ichiro Miki, Nobuyuki Kishibayashi, Hiromi Nonaka, Etsuo Ohshima, Hito ...1992 Volume 59 Issue 3 Pages 357-364
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSWe examined the binding of [3H]U-46619, a thromboxane A2 agonist, to human and guinea pig platelets and the binding of [3H]SQ 29, 548, a thromboxane A2 antagonist, to human, rat and guinea pig platelets. KW-3635 (sodium (E)-11-[2-(5, 6-dimethyl-l-benzimidazolyl)ethylidene]-6, 11-dihydrodibenz[b, e]oxepin-2-carboxylate monohydrate) concentration-dependently inhibited the [3H]U-46619 binding to human and guinea pig platelets with inhibition constants of 1.2 nM and 2.7 nM, respectively. KW-3635 also potently inhibited the [3H]SQ 29, 548 binding to human and guinea pig platelets with inhibition constants of 1.9 nM and 3.2 nM, respectively. In contrast, KW-3635 was less active against thromboxane A2/prostaglandin H2 receptors in rat platelets with an inhibition constant of 97 nM. KW-3635 at 10-5 M did not antagonize various receptors including prostaglandin E2, prostaglandin I2 and neurotransmitters. In addition, 10-5 M KW-3635 did not alter the prostaglandin D2-induced cAMP accumulation in EBTr cells. KW-3635 was inactive towards thromboxane synthase, cyclooxygenase and prostaglandin I2 synthase up to 10-5 M. KW-3635 slightly inhibited 5-lipoxygenase with an IC50 value of 71 μM. These data indicate that KW-3635 is a potent and selective non-prostanoic thromboxane A2 antagonist, and it can recognize the species differences in thromboxane A2/prostaglandin H2 receptors.View full abstractDownload PDF (540K) -
Susumu Matsuda, Hiroshi Saito, Nobuyoshi Nishiyama1992 Volume 59 Issue 3 Pages 365-370
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSBasic fibroblast growth factor (bFGF) was injected with dissociated substantia nigral cells into the striatum of rats prepared by unilateral lesion of the nigrostriatal pathway with 6-hydroxydopamine. The transplanted cells with 5 and 50 ng bFGF reduced the apomorphine-induced rotations by 40 and 30%, respectively, while the decrement of rotations was only 15% in the grafted control without bFGF. Immunohistochemical staining with anti-tyrosine hydroxylase antibody showed that bFGF also tended to increase the number of grafted catecholaminergic neurons along the tracts. In the case of 50 ng bFGF treatment but not 0 or 5 ng bFGF treatment, however, severe gliosis was detected along the grafted region by staining of anti-glial fibrillary acidic protein antibody. These immunohistochemical studies suggested that high-dose bFGF induced extensive gliosis, which might affect the survival of the grafted neurons.View full abstractDownload PDF (1043K) -
Akio Namimatsu, Koichiro Go, Taeko Hata1992 Volume 59 Issue 3 Pages 371-377
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSWe stated that SART-stressed guinea pigs showing nasal mucosal hypersensitivity would serve as an animal model for the in vivo evaluation of antiallergic drugs. In the present study, the mode of action of Neurotropin on nasal allergy compared with those of antiallergic drugs was studied by using SART-stressed guinea pigs. Daily administrations of Neurotropin improved the methacholine-induced hypersecretion and histamine-evoked sneeze response, which are parameters of nasal mucosal hypersensitivity, and increased the density of muscarinic ACh receptors located on the nasal mucosa caused by SART stress. In addition, the inhibitory action on nasal secretion in a passively sensitized model was more intense in SART-stressed guinea pigs than in normal ones. Ketotifen and tranilast were also found to have marked effects on nasal secretion in the passively sensitized SART-stressed model, but only had weak effects on nasal mucosal hypersensitivity. Neurotropin significantly potentiated the action of ketotifen or tranilast. Thus, at least part of the inhibitory effect of Neurotropin on nasal symptoms such as watery secretion and sneezing is thought to have been brought forth through the regulatory action on nasal mucosal hypersensitivity, and its combined use with antiallergic drugs would be a very effective therapeutic regimen for nasal allergy.View full abstractDownload PDF (487K) -
Shigeki Hashimoto, Masafumi Oshita, Kouji Morikawa, Hideo Kato, Yasuo ...1992 Volume 59 Issue 3 Pages 379-385
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSThe pharmacological profile of HSR-175, a new α1-adrenoceptor antagonist, was studied in vitro and compared with those of other α1-antagonists. HSR-175, prazosin, bunazosin and yohimbine competitively antagonized the contractile responses induced by noradrenaline in the dog mesenteric arteries and the rabbit thoracic aorta. The pA2 values for HSR-175 in the dog mesenteric arteries and the rabbit aorta were 10.38 and 9.63, respectively, which were significantly higher than those for prazosin (8.39 and 8.80), bunazosin (8.44 and 8.75) and yohimbine (7.34 and 6.10). HSR-175 also inhibited the sympathetic adrenergic contraction induced by electrical transmural stimulation in the dog mesenteric arteries, and the inhibitory effect of HSR-175 was more potent than those of prazosin and bunazosin. Although HSR-175 also possessed competitive antagonist properties at pre and postsynaptic α2-adrenoceptors in the rat vas deferens and the dog saphenous veins, those affinities (pA2 = 6.41 and 7.05) were much lower than those at postsynaptic α1-adrenoceptors. Furthermore, HSR-175 at concentration of 10-6 M showed no inhibition on the contractile responses to 5-HT, histamine, KCl and angiotensin II in the rabbit thoracic aorta. These results indicate that HSR-175 is a very potent and selective α1-adrenoceptor antagonist.View full abstractDownload PDF (425K) -
Masaaki Hirouchi, Hiroshi Mizutani, Yasuko Kohno, Kinya Kuriyama1992 Volume 59 Issue 3 Pages 387-391
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSCharacteristics of the association of brotizolam, a thieno-triazolo diazepine derivative, to central benzodiazepine receptors were examined. Brotizolam significantly displaced the [3H]flunitrazepam and [3H]β-carboline carboxylate ethylester bindings to crude synaptic membrane from the rat brain. This agent had the highest affinity for benzodiazepine receptors in the cerebellum, and it was found to be 2.1 times that in the spinal cord. Furthermore, a low concentration of brotizolam potentiated the GABA-stimulated 36Cl- influx into membrane vesicles. In contrast, the bindings of [3H]8-hydroxy-2-(di-n-propylamino) tetralin to 5-hydroxytryptamine1A receptors and [3H]ketanserin to 5-hydroxytryptamine2 receptors were not affected by brotizolam. The present results suggest that brotizolam may be a selective and high affinity ligand for the type I central benzodiazepine receptor. The anxiolytic and hypnotic actions of brotizolam seem to be not due to the association with 5-hydroxytryptamine receptor, but due to the activation of the GABAA receptor complex. Furthermore, the present results suggest that the lower affinity of brotizolam to benzodiazepine receptors in the spinal cord than those in the cerebellum may be related to the low muscle relaxation action of this drug.View full abstractDownload PDF (345K) -
Hisashi Kuribara, Sakutaro Tadokoro1992 Volume 59 Issue 3 Pages 393-398
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSEthanol disrupted the discrete lever-press and shuttle avoidances in mice at doses over 1.6 and 2.4 g/kg, p.o., respectively, eliciting a dose-dependent decrease in the % of avoidance with no significant change or slight increase in the response rate. Caffeine increased the response rate of both the avoidances at the doses of 1-30 mg/kg, p.o., but disrupted the avoidance at 100 mg/kg. Caffeine (10 mg/kg) reduced the decreased % of avoidance by ethanol (1.6 and 2.4 g/kg) with a significant increase in the response rate. In contrast, the % of avoidance was significantly lower after the combined administration of ethanol (3.2 g/kg) with caffeine than after ethanol (3.2 g/kg) alone. Unlike ethanol, diazepam (2 mg/kg, s.c.) and pentobarbital (10 mg/kg, s.c.) significantly decreased both the response rate and the % of avoidance. Caffeine (10 mg/kg) ameliorated the decreased response rate and the % of avoidance produced by diazepam and pentobarbital. The present results suggest that caffeine does not effectively ameliorate, but rather may worsen the ethanol intoxication.View full abstractDownload PDF (466K) -
Masakatsu Takahashi, Shogo Tokuyama, Hiroshi Kaneto1992 Volume 59 Issue 3 Pages 399-404
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSWe examined how the ginseng extract (GE) acts on the antinociceptive effect induced by footshock (FS)-, psychological (PSY)- and forced swimming (SW)-stress (stress-induced analgesia, SIA), and also on the suppression by FS- and PSY-stress of the development of tolerance to morphine in mice. Neither an acute treatment nor 5 daily pretreatments with GE at 100 mg/kg, p.o. affected each SIA. Pretreatment with GE at 100 mg/kg, p.o. for 5 days followed by the treatment in combination with the exposure to stresses for another 5 days caused no appreciable changes in the development of tolerance to FS and SW-SIA, but suppressed the development of tolerance to PSY-SIA. When mice were pretreated with GE for 5 days and given GE daily prior to morphine at 10 mg/kg/day, with stress exposure for another 5 days, the inhibitory effect of FS-stress on the development of tolerance to morphine was completely eliminated. The present results suggest that GE, by improving the general metabolism in the body, directs toward normalization of the adaptability which is impaired by stress exposure, while not compromising morphine antinociceptive activity or the SIA, another adaptability produced in confrontation to abnormal environmental stimuli. In addition, the differences in the mechanism underlying the FS- and PSY-stress effect which we have previously demonstrated are also reconfirmed.View full abstractDownload PDF (347K) -
Katsuhiko Miyazawa, Takashi Mikami, Katsuhiko Miyasaka, Shigeru Aonuma1992 Volume 59 Issue 3 Pages 405-411
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSAcute and chronic sialoadenitis were induced in ovalbumin-immunized guinea pigs by a single or repeated (once a day for 5 days) instillation of antigen into the parotid gland via the parotid duct. The acute sialoadenitis was characterized by infiltration of inflammatory polymorphonuclear leukocytes and the chronic one, by extensive tissue destruction together with infiltration of mononuclear leukocytes. In acute sialoadenitis, myeloperoxidase activity in the parotid gland, which was a marker of accumulation of neutrophils, was elevated, but in the chronic stage, it returned nearly to the control level. This observation is in accord with the histological findings that infiltrating cells in acute and chronic sialoadenitis were mainly polymorphonuclear and mononuclear leukocytes, respectively. Although cyclophosphamide suppressed the inflammation, both in acute and chronic sialoadenitis, indomethacin exerted its anti-inflammatory effect only in the acute stage. Our experimental models of acute and chronic sialoadenitis were easy to prepare, and had a high incidence. As the typical features of inflammatory development from acute to chronic phases were observed in these models, these models may be useful for studying the mechanism of the chronic course in immunologically induced inflammation and the effects of drugs on each phase and the chronic course of inflammation.View full abstractDownload PDF (612K) -
Masahiko Ogihara1992 Volume 59 Issue 3 Pages 413-416
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSThe effects of nifedipine and nicardipine on glucagon-stimulated gluconeogenesis from lactate were examined in primary cultures of rat hepatocytes. Nifedipine and nicardipine (10-7 - 10-5 M) significantly potentiated the glucagon-stimulated gluconeogenesis from lactate by increasing intracellular cAMP levels. In contrast, diltiazem and verapamil did not potentiate the glucagon-stimulated gluconeogenesis. 1-Methyl-3-isobutylxanthine and papaverine also potentiated the glucagon-stimulated gluconeogenesis from lactate. On the basis of these results, possible mechanisms by which nifedipine and nicardipine potentiate the glucagon-stimulated gluconeogenesis will be discussed.View full abstractDownload PDF (260K) -
Sachiko Oh-ishi, Kohji Yamaki, Mitsuhiro Abe, Hiroshi Tomoda, Satoshi ...1992 Volume 59 Issue 3 Pages 417-418
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSTriacsin C was previously reported to inhibit long-chain acyl-CoA synthetase and to reduce the production of acyl-CoA in rat neutrophils dose and time-dependently. We found that preincubation with triacsin C inhibited the incorporation of labeled arachidonic acid into rat neutrophils. Furthermore, when triacsin C-treated neutrophils were stimulated with the Ca-ionophore A23187, they released an increased amount of eicosanoids into the culture medium. These results indicate that triacsin C suppressed acylation of arachidonic acid, which resulted in an increase in its metabolites.View full abstractDownload PDF (141K) -
Tsuneyuki Yamamoto, Masuo Ohno, Shin-ichi Yatsugi, Yasuhiro Fujikawa, ...1992 Volume 59 Issue 3 Pages 419-421
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSThe effects of various nootropic candidates on mescaline-induced head-twitches were studied in mice. The number of head-twitches induced by mescaline (100 mg/kg, s.c.) was significantly reduced by idebenone (32 and 100 mg/kg, i.p.), minaprine (0.32-10 mg/kg, p.o.) and nebracetam (100 mg/kg, p.o.). Cholinesterase inhibitors such as tetrahydroaminoacridine (1 and 10 mg/kg, p.o.), NIK-247 (10 and 18 mg/kg, p.o.) and physostigmine (0.32 mg/kg, i.p.) also suppressed the head-twitch response to mescaline. These results suggest that the direct or indirect cholinergic-activating effects of these drugs may be involved in inhibiting mescaline-induced head-twitches.View full abstractDownload PDF (164K) -
Shogo Tokuyama, Ki-Wan Oh, Hack-Seang Kim, Masakatsu Takahashi, Hirosh ...1992 Volume 59 Issue 3 Pages 423-425
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSDaily repeated administration of methamphetamine (MAP) developed reverse tolerance to its ambulation-accelerating effect. After pretreatment of mice daily with ginseng extract (GE) for 5 days, concomitant injections of MAP and GE suppressed the development of reverse tolerance to the effect of MAP, although GE itself did not affect the spontaneous motor activity of the naive mice. These results provide evidence that GE may be useful for prevention and therapy of the adverse action of MAP.View full abstractDownload PDF (164K)
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