Folia Pharmacologica Japonica
Online ISSN : 1347-8397
Print ISSN : 0015-5691
ISSN-L : 0015-5691
Volume 89, Issue 1
Displaying 1-6 of 6 articles from this issue
  • Yasuo SASAKI, Noriko NAGAI, Tsutomu OKIMURA, Itaru YAMAMOTO
    1987 Volume 89 Issue 1 Pages 1-7
    Published: 1987
    Released on J-STAGE: February 23, 2007
    JOURNAL FREE ACCESS
    We used lumin (4, 4'-{3[2(1-ethyl-4-(1-H)quinolidene) ethylidene]} propenylene [bis(1-ethyl quinolinium iodide)]) as a photosensitive cyanin dye and studied its effects on various allergic reactions. We obtained the following results: 1) Lumin slightly inhibited the production of IgE antibody, but showed no effect on the production of IgM and IgG antibodies. 2) Lumin slightly inhibited homologous rat PCA at 48 hr. It also showed some inhibitory activity against histamine (His) release caused by in vitro antigen-antibody reaction. 3) Lumin significantly inhibited the acceleration of the delayed-type hypersensitivity (DTH) reaction by cyclophosphamide (CY). The above results suggest that lumin shows anti-allergic activity through the mediation of immunopharmacological activity.
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  • Yasuo SASAKI, Noriko NAGAI, Tsutomu OKIMURA
    1987 Volume 89 Issue 1 Pages 9-13
    Published: 1987
    Released on J-STAGE: February 23, 2007
    JOURNAL FREE ACCESS
    Lumin was administered at doses of 0.1 to 100 μg/kg for 5 months to NZB/W F1 mice as the model animal for studying systemic lupus erythematosus (SLE), a human autoimmune disease. The increase in anti-thymic autoantibody level was significantly inhibited at doses of 1 to 100 μg/kg. Also, the induction of suppressor T cells by concanavalin A was significantly promoted. In addition, recovery activity was significantly observed, overcoming the reduction in plaque-forming cell (PFC) response of anti-sheep erythrocytes at a dose of 100 μg/kg, as well as the reduction in PFC response of anti-trinitrophenylated-lipopolysaccharide at doses of 0.1 to 100 μg/kg. The above results prove that lumin exhibits an immunomodulating effect against immune disease in mice.
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  • Hideo NAKAMURA, Satoru MOTOYOSHI, Katsumi ISHII, Yasuhiro SETO, Atsuko ...
    1987 Volume 89 Issue 1 Pages 15-24
    Published: 1987
    Released on J-STAGE: February 23, 2007
    JOURNAL FREE ACCESS
    In order to ascertain the mode of anti-inflammatory action of a topical non-steroidal anti-inflammatory drug, etofenamate which is a diethylene glycol ester of flufenamic acid, the in vitro tests for the mechanism of the action were carried out. Etofenamate (3μM) was hydrolysed to flufenamic acid at a rate of 39.5% and 57.0% of the dose during 30 and 60 min incubation, respectively, when incubated with rat peritoneal macrophages stimulated with starch and bacto peptone in phosphate-buffered saline. PGE2 generation by these cells in MEM medium was dose-relatedly inhibited with etofenamate as well as flufenamic acid at the dosage range of 1 to 30μM. This suggests that unchanged etofenamate is active, since the highest conversion rate of etofenamate to flufenamic acid was 15% of the dose during the incubation. Etofenamate produced a dose-related inhibition against lipoxygenase prepared from peritoneal polymorphonuclear leucocytes of guinea pigs, and its activity (IC50=5.3 × 10-5 M) was stronger than that of caffeic acid; flufenamic acid was inactive. Inhibitory activity of etofenamate was one-third or less that of flufenamic acid against the hypotonic-hyperthermic lysis of rat erythrocytes and heat-denaturation of bovine serum albumin. From these results, it was suggested that topically applied etofenamate produces its anti-inflammatory action through prostaglandin synthesis inhibition by flufenamic acid produced in the inflammatory tissue and inhibition of prostaglandin synthesis by macrophages and lipoxygenase inhibition by unchanged etofenamate.
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  • Toshiji MIYAGAWA, Ryuichiro ANDOH, Shinobu SAKURADA, Tsukasa SAKURADA, ...
    1987 Volume 89 Issue 1 Pages 25-31
    Published: 1987
    Released on J-STAGE: February 23, 2007
    JOURNAL FREE ACCESS
    Effects of capsaicin on spontaneous unit discharges in the amygdala single neurons were studied in 26 gallamine immobilized adult cats. Single units were recorded from the amygdala using a stainless steel microelectrode. Of 63 amygdala neurons, 34 were responsive to both noxious (pinching the skin with toothed forceps) and innoxious (tap and/or hair bending) stimuli, 11 were responsive to only innoxious stimuli and the others did not respond to these stimuli. Of 34 neurons responsive to both noxious and innoxious stimuli, 20 were responsive to both bradykinin and capsaicin, and 7 were responsive to only capsaicin. All neurons responsive to bradykinin were also responsive to capsaicin. All neurons responsive to only innoxious stimuli responded to neither bradykinin nor capsaicin. The latency for bradykinin and capsaicin was 8.05 ± 0.92 sec and 1.21 ± 0.33 sec, respectively. The duration for bradykinin and capsaicin was 14.72 ± 1.78 sec and 26.22 ± 4.16 sec, respectively. The increase in firing frequency produced by capsaicin was depressed by morphine (1 mg/kg, i.v.). These depressant effects of morphine on the amygdala neurons were antagonized by naloxone (0.2 mg/kg, i.v.).
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  • Akihiko KUWAHARA, Arata KUBOTA, Masano HAKKEI, Keiji NAKAMURA
    1987 Volume 89 Issue 1 Pages 33-46
    Published: 1987
    Released on J-STAGE: February 23, 2007
    JOURNAL FREE ACCESS
    Aniracetam, 1-p-anisoyl-2-pyrrolidinone, is known to be a nootropic or cognitive activator. Aniracetam protects against memory and learning deficits without causing effects on motor function and the autonomic nervous system. A drug dependence study on aniracetam utilizing the intragastric route of administration was performed in male cynomolgus monkeys. The behavioral observation test after acute administration revealed that aniracetam at the dose of 25 ?? 400 mg/kg did not change the gross behavior. In the self-administration initiation test, animals were exposed to two or three unit doses of aniracetam and references for a total available period of 7 weeks. Aniracetam at the dose of 25, 50 and 75 mg/kg/injection did not initiate self-administration in the respective group of 4, 4 and 2 animals. In the study with d-methamphetamine hydrochloride at the dose of 0.1 mg/kg/injection, 1 out of 4 animals started to consistently self-administer the drug. Self-administration of cocaine hydrochloride at the dose of 10 mg/kg/injection was confirmed in 3 out of 5 animals, and these 3 animals died from overdosing later. In the physical dependence direct induction test, animals received aniracetam (50 mg/kg) and sodium pentobarbital (25 mg/kg: the dose inducing intermediate CNS depression) intragastrically twice a day for 31 consecutive days. Abrupt withdrawal of aniracetam did not elicit abstinent signs (including changes in appetite and body weight) in all 6 animals, whereas withdrawal of pentobarbital produced typical abstinent behavioral signs and decreases in appetite and body weight. In conclusion, aniracetam was confirmed to develop neither physical dependence nor psychic dependence in cynomolgus monkeys.
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  • Hiroyuki SONOKI, Yasumi UCHIDA, Masatoshi MASUO, Takanobu TOMARU, Akih ...
    1987 Volume 89 Issue 1 Pages 47-53
    Published: 1987
    Released on J-STAGE: February 23, 2007
    JOURNAL FREE ACCESS
    Effects of α-human atrial natriuretic polypeptide (α-hANP) on a model of congestive heart failure (CHF), we established in dogs, were investigated. The model was made by protease injection into the left ventricular free wall, saline loading, and dextran and methoxamine infusion. By this maneuver, left atrial pressure (LAP), systemic vascular resistance (SVR) and left ventricular end-diastolic pressure (LVEDP) were markedly increased, aortic blood flow (AoBF) was decreased and systemic blood pressure (SBP) was unchanged. Following intravenous application of 0.50 μg/kg α-hANP, LAP was reduced from 18.9 to 14.0 mmHg (N =7, mean) ; SBP, from 114.4 to 105.1 mmHg; SVR, from 21603 to 15602 dyne sec/cm5; and LVEDP, from 22.2 to 17.6 mmHg; while AoBF was increased from 0.46 to 0.54l/min. Vmax and T were little influenced. The results indicate that α-hANP improved canine CHF mainly through its vasodilating action.
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