Folia Pharmacologica Japonica
Online ISSN : 1347-8397
Print ISSN : 0015-5691
ISSN-L : 0015-5691
Volume 81, Issue 2
Displaying 1-7 of 7 articles from this issue
  • Nobuo HARADA
    1983 Volume 81 Issue 2 Pages 105-113
    Published: 1983
    Released on J-STAGE: March 07, 2007
    JOURNAL FREE ACCESS
    Asebotoxin III (ATX-III), a diterpenoid isolated from the leaves of Asebi, Pieris japonica, was found to produce hemorrhage into the lungs when the toxin in a dose of 2 ?? 8 μg was injected into the lateral ventricle of guinea pigs under urethane anesthesia (0.8 g/kg, i.p.). The occurrence of the lung hemorrhage was associated with a hypertensive response which was two times higher than the control level. The hemorrhage first occurred at a time when systemic blood pressure reached its highest level. This was verified by X-ray examination on the chest of the guinea pig. In contrast to the hemorrhage into the lungs, the other organs in the abdominal cavity were found to be rather ischemic in the autopsy cases. Death due to hemorrhage into the lungs was effectively prevented by pretreating the guinea pigs with phentolamine mesylate (1 mg/kg, i.v.) and 6-hydroxy-dopamine hydrobromide (40 mg/kg, i.p.). Time before death was significantly prolonged by treating the animals with reserpine (5 mg/kg, i.m.), chlorpromazine hydrochloride (10 mg/kg, i.v.), guanethidine sulfate (20 mg/kg, i.v.), and hexamethonium bromide (5 mg/kg, i.v.), though death from the lung hemorrhage was not completely blocked. The hemorrhage was aggravated by pretreatment with atropine sulfate (5 mg/kg, i.v.). EEG recordings from the hypothalamus of guinea pigs with ATX-III injection showed an exciting pattern of waves of high frequency and spike discharge. On the mechanisms for the lung hemorrhage induced by ATX-III, we concluded that the toxin produced depolarization of some neurones in the hypothalamus, thereby provoking massive sympathetic discharge for producing severe pulmonary hypertension and hemorrhage.
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  • Hideomi FUKUDA, Masayoshi GOTO, Mitsuru KONDO, Tetsu UCHIGASAKI, Yuko ...
    1983 Volume 81 Issue 2 Pages 115-126
    Published: 1983
    Released on J-STAGE: March 07, 2007
    JOURNAL FREE ACCESS
    Antiarrhythmic actions of lorcainide were compared with those of disopyramide on different types of arrhythmias in animal models. It was shown in dogs that lorcainide and disopyramide were approximately equipotent against the arrhythmias following coronary occlusion. In guinea pigs, lorcainide was less effective than disopyramide against the ouabain-induced arrhythmia. Both drugs showed a weak protective action against the aconitine-induced ventricular arrhythmias, but had no effect on the cardiac arrest. In the arrhythmias induced by the application of acetylcholine on the right auricle of guinea pigs, the disappearance of P-waves and the disturbance of R-R intervals were inhibited by disopyramide, but lorcainide had no influence on these events; both prevented the atrial fibrillation induced by acetylcholine application. Both drugs by themselves induced ventricular arrhythmias in guinea pigs.
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  • Takahiko SUZUKI, Kensuke KISARA, Kenji ONODERA, Yasumi OGURA
    1983 Volume 81 Issue 2 Pages 127-134
    Published: 1983
    Released on J-STAGE: March 07, 2007
    JOURNAL FREE ACCESS
    The effect of cholinergic drugs on the tremor induced by subcutaneous (s.c.) injection of a 1 v/v% phenol solution was investigated. Male dd-Y strain mice weighing 18-24 g were used in all experiments. Intraperitoneal (i.p.) administration of physostigmine (0.05-0.1 mg/kg) did not alter the tremor. Neostigmine (0.05-0.1 mg/kg i.p.) increased the strength of the tremor weakly and shortened the latency of the tremor. I.p. administrations of methacholine, atropine, methylatropine, and scopolamine did not produce significant effects on the tremor. I.p. injection of nicotine (0.5-1 mg/kg) shortened the duration of the tremor. Intracerebro-ventricular (i.c.v.) infusions of nicotine (4 μg/mouse) and carbachol (5 μg/mouse) prolonged the latency of the tremor. Furthermore, i.c.v. infusion of nicotine (4 μg/mouse) reduced the strength of the tremor slightly. On the contrary, i.p. (10-20 mg/kg) or i.c.v. (20-60 μg/meuse) administration of mecamylamine potentiated the strength and prolonged the duration of the tremor in a dose dependent manner. Hexamethonium (10-20 μg/mouse, i.c.v.) also potentiated the strength and prolonged the duration of the tremor. These results suggest that a peripheral increase of acetylcholine level may potentiate the tremor induced by phenol, and the tremor may be suppressed by a negative feedback mechanism involving the nicotinic cholinergic system of the central nervous system.
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  • Hiroyuki YOSHIMURA, Nobuya OGAWA
    1983 Volume 81 Issue 2 Pages 135-141
    Published: 1983
    Released on J-STAGE: March 07, 2007
    JOURNAL FREE ACCESS
    The present study was conducted to investigate the effect of ethylalcohol on agonistic behavior using a residentintruder paradigm. In this paradigm, a resident male mouse has been cohabiting with a female for 5 weeks, and an intruder male mouse is introduced into the resident's home cage. The effects of four doses of ethylalcohol (vehicle, 0.5, 1.0, and 2.0 g/kg, p.o.) were assessed in resident mice and group-housed intruder mice. Residents and intruders were drugged on alternate test days, and all animals received different sequences of drug conditions according to a random schedule. When resident mice were treated with ethylalcohol biphasic effects on resident's aggressive elements were observed: 0.5 and 1.0 g/kg of ethylalcohol increased attack bitings and sideways posture, while 2.0 g/kg of the drug suppressed aggressive elements. On the other hand, when intruder mice were drugged the resident's attack bitings were significantly increased in a dose-dependent manner. At this time, defensive upright postures of intruder mice were suppressed by the drug. Ethylalcohol at the employed doses did not affect locomotor activity in both resident and intruder mice. The results suggest that ethylalcohol enhances the hostility of resident to the intruding animal and suppresses the anxiety of an intruder to the attacking animal.
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  • Fumio KIMURA, Shoko FUKAZAWA, Fumiko SAITO, Kayo SHONAI, Setsuya TAKEU ...
    1983 Volume 81 Issue 2 Pages 143-148
    Published: 1983
    Released on J-STAGE: March 07, 2007
    JOURNAL FREE ACCESS
    Effects of noradrenaline and isoproterenol on insulin secretion in rat pancreas have been studied by means of the in situ perfusion method described previously. Noradrenaline: The insulin secretion from the rat pancreas perfused with the high glucose buffer decreases after the administration of 1 μg/0.1 ml of noradrenaline into the perfusion fluid. These noradrenaline-induced hyposecretions can be reversed by pretreatment with phentolamine (10 μg/ml), while they are potentiated after propranolol (10 μg/ml) pretreatment. Isoproterenol : The insulin secretion from the rat pancreas perfused with the same buffer increases after the administration of 1 μg/0.1 ml of isoproterenol into the perfusion fluid. These isoproterenol-induced hypersecretions are found to be potentiated after pretreatment with phentolamine or propranolol, and atropine (100 μg/ml) pretreatment does not produce any changes in the isoproterenol-induced hypersecretion. These results suggest that the β-receptors on the B-cells stimulate the insulin secretion and the β-receptors on the D-cells decrease them. This communication gives a short discussion of whether α-receptors may be on D-cells or not.
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  • Toshio KASAMA, Yuichi FUJII, Yoko AIDA, Kiyoshi MAYUZUMI, Yoko MAYUZUM ...
    1983 Volume 81 Issue 2 Pages 149-165
    Published: 1983
    Released on J-STAGE: March 07, 2007
    JOURNAL FREE ACCESS
    Differences between the pharmacological effects of bromazepam given by oral and rectal administration were investigated in mice and rats. 1) Bromazepam dose-dependently prolonged the sleeping time induced by thiopental-Na, ethanol and ether by both administration routes. 2) The analgesic action of bromazepam was recognized by the hot-plate method and the algolytic test. In the hot-plate test, analgesic actions of morphine and pentazocine were potentiated by bromazepam in a dose of 0.5 mg/kg by both routes. 3) The muscle relaxant effect of bromazepam administered rectally was more potent than that administered orally in the inclined screen test and the rotarod test. This effect of bromazepam by rectal administration was approximately 2 times as potent as that by oral administration. 4) Bromazepam inhibited the convulsion induced by maximum electric shock, pentylenetetrazol and picrotoxin. In pentylenetetrazol-induced convulsion, the inhibitory effect of bromazepam administered rectally was 2 times as potent as that administered orally. In the other convulsion test, no significant differences between oral and rectal administration could be recognized. 5) Hyperemotionality and muricide (mouse-killing behaviour) of rats with bilateral olfactory bulb ablations (OB rat) were reduced by oral and rectal administrations of bromazepam in a dose-dependent manner. The effects by rectal administration were more potent than that by oral administration. Bromazepam was approximately 20 times as potent as diazepam administered by the same route. Fighting behaviour in mice subjected to footshock was suppressed by rectal administration of bromazepam, and this effect was as same as that by oral administration. 6) The rate of lever pressing response in the lateral hypothalamic self-stimulation test in the Skinner box was markedly increased by rectal administration of 0.2 mg/kg bromazepam. 7) Methamphetamine-induced hyperactivity of mice was significantly suppressed only by bromazepam administered rectally in a dose of 5 mg/kg. 8) The falling effect of bromazepam on body temperature in normal rats was the same in both administration routes and was dose-dependent. From these data, significant differences of the pharmacological effects between oral and rectal administration of bromazepam were recognized in the duration of action and, in part, potencies; and therefore, rectal administration of bromazepam may be a useful dosage form for clinical use.
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  • Kazunaga FUKAWA, Noriyuki MISAKI, Osamu KAWANO, Masayuki UCHIDA, Shige ...
    1983 Volume 81 Issue 2 Pages 167-174
    Published: 1983
    Released on J-STAGE: March 07, 2007
    JOURNAL FREE ACCESS
    The following results were obtained as the result of the sequential observations with an endoscope of the gastric ulcer produced by submucosal injection of acetic acid in rats. 1) The size of the ulcer produced by acetic acid injection observed on the 3rd day after ulcer induction depended on the concentration and volume of acetic acid. 2) The natural reducing rates of the size of ulcers in the region between the fundus and pylorus on the anterior wall (A) and in the glandular region on the greater curvature (B) were compared. The reducing rate of B ulcer was significantly faster than that of A ulcer. 3) No significant difference was observed in the reducing processes of untreated ulcers in 7 weeks old rats and 25 weeks old rats. 4) The ulcer reducing rate of female rats was found to be slightly faster than that of male rats. 5) The ulcer reducing rates of the aldioxa (ALD) and sucralfate (SUC) treated group were significantly faster than that of the control group. However, no difference in the ulcer reducing process between the cimeitdine (CIM) treated group and the control group was observed. 6) The ulcer indices (UI) of both the combinations of ALD and SUC and of ALD and CIM were found to be significantly less than that of the control group on the 20th day. Treatment with drug combinations shortened the healing period of ulcers more than treatment with one drug alone. The percent healing by the combination of ALD and SUC was the highest among the groups treated. 7) An approximately linear relationship exists between the logarithm of the days after ulcer induction (x) and logarithm of UI (y), and the following equation was obtained: log y=a log x + b. Slope (a) indicates the ulcer reducing rate in evaluating the ulcer reducing process.
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