Folia Pharmacologica Japonica
Online ISSN : 1347-8397
Print ISSN : 0015-5691
ISSN-L : 0015-5691
Volume 96, Issue 5
Displaying 1-7 of 7 articles from this issue
  • Yoshitsugu OSUMI
    1990 Volume 96 Issue 5 Pages 205-216
    Published: 1990
    Released on J-STAGE: February 20, 2007
    JOURNAL FREE ACCESS
    Central neurotransmitter and/or neuromodulator candidates reported to affect gastric acid secretion are: (excitatory) acetylcholine, thyrotropin releasing hormone, GABA, oxytocin; (inhibitory) noradrenaline, adenosine, bombesin, calcitonin-gene related peptide, corticotropin releasing factor, beta-endorphin, neurotensin, neuropeptide Y, insulin-like growth factor II and prostaglandins. Regulation of gastric acid secretion by central administration of these substances in experimental animals such as rats and dogs are briefly reviewed, and central inhibitory mechanisms of this function are discussed based on our studies with noradrenaline and bombesin. Roles of hypothalamic nuclei such as the ventromedial nucleus and the lateral hypothalamus in regulation of autonomic nerve activities are also described as an introductory note.
    Download PDF (10165K)
  • Jun NAGURA
    1990 Volume 96 Issue 5 Pages 217-225
    Published: 1990
    Released on J-STAGE: February 20, 2007
    JOURNAL FREE ACCESS
    Experiments were carried out to get information about the shifting mode of the frequency-force relationship curve (FFRC) of several well-established agents in guinea pig ventricular myocardium to estimate the ionic mechanism of inotropic action. The increase in [Ca2+]o or decrease in [Na+]o shifted the FFRC to the left and upwards, but no shift was observed when [Ca2+]o/ [Na+]o2 ratio was kept constant. Drugs increasing [Na+]1 (veratridine, asebotoxin) caused a parallel leftward shift of FFRC in the middle range of contraction frequency. Tetrodotoxin depressed the force of contraction (Fc) at higher frequencies, reflecting the fast Na influx inhibition. Nifedipine depressed, while BAY K 8644 augumented, the Fc at all frequency ranges, reflecting the Ca influx modulation. Ouabain and [c-AMP]1-elevating agents (isobutyl methylxanthine, histamine) strengthened the Fc at all frequencies. The ionic mechanism of these two groups of cardiotonic agents depending primarily on either Na or Ca influx could be estimated from a distinct time difference of the peak in the “rested-state” contraction curves of guinea pig papillary muscle. The shifting pattern of FFRC will contribute to the estimation of the mechanism of inotropic agents.
    Download PDF (7266K)
  • Shigeki FUJISAWA, Nobunari TACHIKAWA, Eiji MURAKAMI, Masashi MASUDA, S ...
    1990 Volume 96 Issue 5 Pages 227-242
    Published: 1990
    Released on J-STAGE: February 20, 2007
    JOURNAL FREE ACCESS
    The effect of LC-80 on infarct size induced by 6 hr coronary occlusion was studied in anesthetized dogs. LC-80 at a dose of 100 mg/kg, i.v. was injected 5 min after coronary occlusion and then infused at a rate of 50 mg/kg, i.v./hr until the heart was excised. The two risk areas were determined both by injecting a fluorescent dye (Thioflavin S) into the left atrium (in vivo) and by perfusing the non-occluded coronary bed with Monastral Blue (in vitro). The infarct size was determined by topographically tracing the area of myocardium unstained by triphenyltetrazolium chloride. Four zones such as Zone 1 (normal tissue), Zone 2 (tissue characterized by collateral blood flow), Zone 3a (tissue developing necrosis), Zone 3b (necrotic tissue) were delimitated. As a result, (1) LC-80 significantly diminished the incidence of ventricular arrhythmias. (2) LC-80 significantly inhibited the decrease in myocardial free carnitine level in Zone 2 and Zone 3b. (3) LC-80 significantly reduced the infarct size expressed as a percentage of the risk area and increased the size of Zone 2. (4) In the electron microscopic findings, LC-80 showed lesser morphological changes such as swollen mitochondria and intracellular and extracellular edema, especially in Zone 2. (5) LC-80 may be useful for inhibiting the evolution of myocardial ischemic cell death both by the protection of ischemic myocardium and presumably by the increase in the collateral blood flow.
    Download PDF (15417K)
  • Tsuyako OHKUBO, Manabu SHIBATA, Hiroshi TAKAHASHI
    1990 Volume 96 Issue 5 Pages 243-253
    Published: 1990
    Released on J-STAGE: February 20, 2007
    JOURNAL FREE ACCESS
    Participation of the sensory neurons, especially substance P (SP)-containing neurons, in the inflammatory response induced by formalin (FOR), croton oil (CRO), mustard oil (MUS), carrageenin (CAR), dextran (DEX) and egg white (EGG) was studied in mice and rats. FOR-induced foot edema was significantly inhibited by denervation of the sciatic nerve of rats, but it was slightly facilitated by that of the saphenous nerve. CAR-induced edema was not influenced by denervation of both nerves. In mice pretreated with capsaicin of the sciatic nerve, the early phase of foot edema induced by FOR, CRO or MUS was significantly inhibited. Edema induced by CAR, DEX or EGG was not inhibited by the capsaicin treatment. Spantide (an SP antagonist) at 0.1 mg/kg showed the same result as the capsaicin treatment. FOR, CRO or MUS caused a marked plasma extravasation, which was inhibited by spantide. The weak plasma extravasation elicited by CAR, DEX or EGG was not inhibited by spantide. FOR, CRO or MUS caused an intense biphasic nociceptive response; and the early phase of the response was inhibited by spantide. CAR, DEX or EGG caused little or no nociception. These findings suggest that SP antidromically released from the primary sensory neurons may induce potent vascular responses such as vasodilatation and plasma extravasation in the early phase of inflammation induced by FOR, CRO and MUS, whereas inflammatory responses induced by CAR, DEX and EGG may progress through different processes.
    Download PDF (8018K)
  • Shigeo OHBAYASHI, Noriyuki MISAKI, Kazuyoshi BANDO, Masayuki UCHIDA, O ...
    1990 Volume 96 Issue 5 Pages 255-263
    Published: 1990
    Released on J-STAGE: February 20, 2007
    JOURNAL FREE ACCESS
    The effects of aldioxa and cetraxate hydrochloride on the formative process of gastritis induced with intragastric application of 2 % sodium hydroxide were studied. Rats were given food including either aldioxa or cetraxate hydrochloride for 6 weeks after the sodium hydroxide application. After sacrifice, the stomachs were removed, and the gastric mucosa were observed macroscopically and histologically. Gastric mucosal injury was widely induced with sodium hydroxide, being histologically characterized by mucosal hypertrophy, cell infiltration and intestinal metaplasia. These lesions seem to be the early stage of chronic gastritis. The aldioxa group showed a decrease of mucosal hypertrophy and cell infiltration as compared with the control group. In the cetraxate hydrochloride group, the mucosal surface of white gray color and the mucosal bosselation were observed macroscopically. Histologically, these were found to be cell infiltration and cyst formation. Moreover, intestinal metaplasia occurred at high incidence in this group. These findings in the cetraxate hydrochloride group are recognized to be an aggravation of chronic gastritis. From the above results, it is suggested that aldioxa promotes good regeneration of mucosa and should be useful for the clinical therapy of chronic gastritis.
    Download PDF (10119K)
  • Sumio MINEMATSU, Masayuki TAKI, Masahiko WATANABE, Mutsumi TAKAHASHI, ...
    1990 Volume 96 Issue 5 Pages 265-273
    Published: 1990
    Released on J-STAGE: February 20, 2007
    JOURNAL FREE ACCESS
    Shosaiko-to-go-keishikashakuyaku-to (TJ-960) is an extract of nine herbal drugs (Paeoniae radix, Cinna momi cortex, Bupleuri radix, Zingiberis rhizoma, Glycyrrhizae radix, Ginseng radix, Scutellariae radix, Pinelliae tuber and Zizyphi fructus) that has a potent anticonvulsant action. The rat fetuses treated orally with TJ-960 during the organogenesis period (days 7-17 of gestation) revealed no anomalies (up to 3000 mg/kg/day). When TJ-960 was co-administered with sodium valproate (VPA, 400 mg/kg) during the organogenesis period, embryonic resorption, fetal body weight, ossification and skeletal variation or anomalies induced by VPA were markedly reduced. The maternal plasma and embryonic concentration of VPA with TJ-960, however, were not significantly different from VPA alone. These results suggest that TJ-960 has protective effects against the teratogenicity of VPA.
    Download PDF (6604K)
  • Kuninori TAKAGI, Yasuo WATANABE, Takeshi SHIBUYA
    1990 Volume 96 Issue 5 Pages 275-288
    Published: 1990
    Released on J-STAGE: February 20, 2007
    JOURNAL FREE ACCESS
    A new method for measuring the endogenous acetylcholine (ACh) and choline (Ch) levels using a PY/GC/MS was established, and then the alteration of cholinergic neurons in the iminodipropionitrile (IDPN) induced dyskinesia model rat brain was studied. In performing the determinations of small amounts of brain ACh and Ch levels using a curie point PY/GC/ MS, the following points were improved upon in the present study: 1) We shortened the distance between the sample tube and injection port allowing the rapid transformation to an analytical system without sub-reaction and re-synthesis of demethylated products. 2) The suitable pyrolytic temperature (curie point) was adjusted to 333°C. 3) Then the aqueous sample (2 μl) was wrapped in a pyrofoil with a curie point of 333°C followed by drying at 80°C. Subsequently, the pyrofoil was formed by a 200 kgf/cm2 press. 4) A fused silica capillary column (DB-5) was used instead of a pre-packed column (Jenden Phase). By these improvements, both calibration curves of ACh and Ch have high linearities (r=0.988) between 1 pmol and 2 pmol, and the apparent peak of quasi-molecular ion and less fragment ion of each Ch analog was obtained. In the globus pallidus, caudate nucleus, hippocampus and cerebellum of IDPN induced dyskinesia model rats, remarkable reductions of ACh levels were observed using our newly improved PY/GC/MS method. Thus, our improved method can be utilized for measuring ACh levels in small discrete brain regions.
    Download PDF (9510K)
feedback
Top