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Volume 41 (1986)
- Issue 4 Pages 431-
- Issue 3 Pages 267-
- Issue 2 Pages 139-
- Issue 1 Pages 1-
Volume 41, Issue 2
Displaying 1-17 of 17 articles from this issue
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Abdulrahman M. AGEEL1986 Volume 41 Issue 2 Pages 139-145
Published: 1986
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe effects of the tricyclic antidepressants desipramine HCl and chlorimipramine HCl on buprenorphine HCl antinociceptive activity were studied in mice using the hot-plate and the tail-flick methods. In the hot-plate test, desipramine caused a transient antinociceptive effect at low doses, but it decreased buprenorphine analgesia. Chlorimipramine in this test caused a more sustained antinociceptive effect, especially at relatively higher doses, and it did not significantly change buprenorphine analgesia. In the tail-flick test, desipramine either reduced or increased the tail-flick latency in a dose-specific manner, and chlorimipramine (10 mg/kg) significantly increased the tail-flick latency. Desipramine (1 mg/kg) caused a decrease followed by an increase in buprenorphine analgesia. Desipramine (5 and 10 mg/kg) caused significant increases in buprenorphine analgesia. All doses of chlorimipramine (1, 5 and 10 mg/kg) caused significant increases in buprenorphine analgesia. Thus, depending on the test employed, buprenorphine analgesia was modified differently by these tricyclics. Biochemical data suggested a greater role for brain 5-hydroxytryptamine (5-HT) than noradrenaline in tricyclic analgesia.View full abstractDownload PDF (558K) -
Yasumitsu YAMANAKA, Ritsuko TAKANO, Toru EGASHIRA1986 Volume 41 Issue 2 Pages 147-154
Published: 1986
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSRepeated administration of a large dose of methamphetamine (MA) (25 mg/kg, i.p. twice daily for 4 days) to mice enhanced locomotor activity and decreased stereotyped behavior following a subsequent injection of MA. Simultaneous determinations of catecholamines revealed a depletion of brain dopamine. The moderate doses of haloperidol significantly enhanced MA-induced locomotor activity in mice. A significant enhancement of MA-induced locomotor activity was observed in the rats pretreated with 6-hydroxydopamine into the striatum, and this effect correlated negatively with the striatal dopamine level. These results suggest that hypofunction of striatal dopaminergic neuron systems induced by repeated administration of MA may be one of possible mechanisms of the enhancement of MA-induced locomotor activity due to the decrease of stereotyped behavior.View full abstractDownload PDF (593K) -
Masahiro IWAKI, Yoshitaka INO, Akemi MOTOYOSHI, Masayuki OZEKI, Takuo ...1986 Volume 41 Issue 2 Pages 155-162
Published: 1986
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSEffects of FUT-175 on the pancreatic enzymes in vitro and in vivo in the enterokinase-induced experimental acute pancreatitis were investigated, and they were compared with those of gabexate and aprotinin. In in vitro experiments, FUT-175 inhibited the pancreatic protease activities 10 to 100 times more potently than gabexate. Furthermore, FUT-175 inhibited the enterokinase activity. Unlike aprotinin, FUT-175 inhibited α2-macroglobulin bound trypsin activity as well as free trypsin. In in vivo experiments, at doses of 0.5-50 μg/kg/min, FUT-175 suppressed the elevated protease activities in the experimental acute pancreatitis more potently than gabexate. Differently from the action of aprotinin, FUT-175 suppressed trypsin activities both in the pancreas and in the plasma to the same extent. Furthermore, FUT-175 reduced the mortality of rats in the experimental acute pancreatitis in a dose-dependent manner. These data strongly support that FUT-175 is clinically useful in the therapy of acute pancreatitis.View full abstractDownload PDF (670K) -
Norimitsu L. SATO, Sueo NIIMURA, Nobuyoshi FUJISAWA, Yoshitaka MAEDA1986 Volume 41 Issue 2 Pages 163-171
Published: 1986
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSIncrease in vascular permeability is usually seen at the growth site of a tumor implant in murine dermal tissue. Increased vascular permeability was inducible by the subcutaneous injection of a solid tumor extract rich in protein precipitable at 20-50% saturation of ammonium sulfate. The vascular permeability-increasing activity of the tumor extract was reducible in the presence of highly polymerized dextran sulfate (DS-500) which showed a strong anticomplementary activity, but not by other substances such as dextran sulfate with a low molecular weight, non-sulfated dextran, chondroitin sulfate or heparin. As the tumor extract includes γ-globulins in aggregated or bound form and adsorbs complements, it is probable that the aggregated γ-globulins increase vascular permeability by triggering the complement activation system in the skin. DS-500 might antagonize the process.View full abstractDownload PDF (770K) -
Ryo FUJIHARA, Nobuyoshi SUNAGANE, Tsutomu URUNO, Kazuhiko KUBOTA1986 Volume 41 Issue 2 Pages 173-181
Published: 1986
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe effect of phenylephrine, an α-agonist, on the Ca movements and the influence of removal of external Na+ on the relaxant activity of phenylephrine were examined in the taenia coil of guinea pigs. Phenylephrine (10-7-10-5 M) caused dose-dependent relaxation of the taenia coli contracted by 20 mM KCl in Locke-Ringer solution. Phenylephrine (10-5 M) suppressed the spike discharges of the taenia coil evoked by 20 mM KCl without affecting the membrane potential, and this was accompanied by the muscle relaxation. Phenylephrine also inhibited the cellular 45Ca-uptake in the taenia coil, but had no discernible effect on the 45Ca-efflux from the smooth muscle. These effects of phenylephrine were not observed in a Na-free solution or in the highly depolarized smooth muscle. These findings suggest that the inhibition of Ca-influx in the taenia coil may be involved in the phenylephrine-induced relaxation in the partly depolarized tissue. Reasons for reduction of phenylephrine action encountered under the Na-free condition were also discussed.View full abstractDownload PDF (647K) -
Hiroyasu KINEMUCHI, Fumio MORIKAWA, Toshihiko UEDA, Yuichiro ARAI1986 Volume 41 Issue 2 Pages 183-189
Published: 1986
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSIn vitro studies of the effect of MD 780236, a selective monoamine oxidase (MAO)-B inhibitor, on a semicarbazide-sensitive amine oxidase (SSAO) in rat testis and lung showed that this compound dose-dependently inhibited SSAO activity. The extents of inhibition of MAO-A, -B and SSAO in these two rat tissues by this compound after 30 min of preincubation were found to be MAO-B>MAO-A>SSAO. This selectivity was also evident in preparations without preincubation. Degree of inhibition of SSAO was not significantly influenced by pretreatment with either 10-3 M clorgyline, I-deprenyl or 10-4 M SKF 525A. Inhibition of SSAO was not enhanced by varying the time of preincubation of the enzyme and the compound, indicating direct action on and reversible inhibition of SSAO. The inhibition of SSAO by MD 780236 was non-competitive with or without preincubation, with a Ki value of 110 μW. Although MD 780236 is a selective and "suicide substrate" inhibitor of MAO-B, these present results indicate that this compound may also inhibit SSAO activity, but by a mechanism different from that for MAO-B. These findings confirm an earlier hypothesis that compounds that inhibit both MAO and SSAO have totally different modes of action on these two different amine oxidases.View full abstractDownload PDF (531K) -
Yuichiro ARAI, Yoshie TOYOSHIMA, Hiroyasu KINEMUCHI1986 Volume 41 Issue 2 Pages 191-197
Published: 1986
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe α-methylated substrate-analogue monoamines, dl-α-methyltryptamine, dl-α-methylbenzylamine and two optical isomers of α-methylbenzylamine, were shown to be inhibitors of rat lung semicarbazide-sensitive amine oxidase (SSAO), with dl-α-methyltryptamine being the most potent and d-α-methylbenzylamine, the least. The three compounds, dl-α-methyltryptamine and the two isomers of α-methylbenzylamine also inhibited rat brain monoamine oxidase (MAO)-A and -B with a greater selectivity towards MAO-A. Preincubation of rat lung and brain homogenates with either of these compounds revealed that the inhibition of MAO and SSAO is reversible. The modes of inhibition of MAO-A and -B were competitive with the substrates tested. However, inhibition of SSAO by dl-α-methyltryptamine was found to be a mixed type (with a Ki value of 47 μM) and those by the racemic form and two isomers of α-methylbenzylamine were non-competitive (with Ki values of 90 μM for the racemic compound, 1070 μM for the d-isomer and 72 μM for the I-isomer). The present results indicate that SSAO can recognize optical isomers and that some α-methylated monoamines tested in the present study inhibit SSAO with properties different from those as MAO inhibitors.View full abstractDownload PDF (509K) -
Kazuko MURATA1986 Volume 41 Issue 2 Pages 199-203
Published: 1986
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe recovery of the parotid gland in the rat was studied by isoproterenol-induced amylase release from the parotid tissue in vitro after the removal of duct ligation following 2 and 7 days of obstruction. The percentage of amylase release did not change, but the activity of amylase in the medium (the released amylase activity) increased gradually after the removal of ligation. When the duct was ligated for 2 days, a complete recovery of the released amylase activity was seen 21 days after the removal of ligature. However, in the case of 7-day-ligation, the recovery was about 70 percent after the same period. An obstruction of a shorter duration produced a more rapid recovery of amylase release. Amylase activity in the parotid tissue increased gradually with time after the removal of ligature, and the recovery rates were very similar to that of the released amylase activity. The present results suggest that the recovery of released amylase activity after the removal of ligature is due to the increase of amylase content in the parotid tissue.View full abstractDownload PDF (325K) -
Satoshi YUASA, Atsuko SUDOH, Yoshihide NAKAO, Kohei UMEZU1986 Volume 41 Issue 2 Pages 205-210
Published: 1986
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSSince tritoqualine (TRQ) is effective in suppressing the increase of serum transaminases in acute hepatic injured rats induced by some hepatotoxins, protection of the hepatocyte membrane is suggested to be one of the pharmacological effects of TRQ. In the present study, we investigated the effects of TRQ on lipid peroxidation and enzyme leakage caused by carbon tetrachloride (CCl4) exposure in isolated hepatocytes and the liver in vivo, compared with vitamin E. The results were as follows: 1) Hepatocytes isolated from TRQ-administered rats showed less enzyme leakage than those from control rats after CCl4 addition. 2) TRQ displayed strong inhibition of lipid peroxidation in isolated hepatocytes. In comparison with vitamin E, TRQ showed almost the same inhibitory action on lipid peroxidation, but a stronger suppression of enzyme leakage. 3) Vitamin E showed a weaker protection from increase of glutamic oxaloacetic transaminase than TRQ, in spite of its stronger inhibition of lipid peroxidation in vivo. From these results, it is suggested that the membrane protecting action of TRO is partially derived from its suppression of lipid peroxidation, but "another action" may also play an important role in protecting the fragile membrane.View full abstractDownload PDF (510K) -
Katsuhiko TAWARA, Masanao ISHIHARA, Hidemasa OGAWA, Munehiro TOMIKAWA1986 Volume 41 Issue 2 Pages 211-222
Published: 1986
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSEffect of probucol, pantethine and their combinations on serum lipoprotein metabolism and on the incidence of atheromatous lesions in aorta and coronary artery was studied in cholesterol-fed rabbits. Probucol treatment (0.5% in diet) resulted in reducing HDL cholesterol and serum apo A-I levels significantly, while pantethine treatment (0.25%-0.75% in diet) tended to increase HDL cholesterol and serum apo A-I levels. Combined treatment with these two drugs showed a significant prevention in the reduction of HDL cholesterol and serum apo A-I levels by probucol alone. Probucol or pantethine treatment reduced effectively (V) LDL cholesterol and serum apo B levels, and these effects were accelerated additively when the two drugs were given concurrently. Atheromatous lesions in aorta and coronary artery in cholesterol-fed rabbits were prevented by the treatment with probucol (0.5% in diet) or pantethine (0.75% in diet) for 24 weeks. The combined treatment with these two drugs showed more marked prevention than either drug alone. From these findings, it is concluded that the combined treatment of probucol with pantethine is effective for improvement of serum lipoprotein disorders and for prevention of the incidence of atheromatous lesions in aorta and coronary artery in cholesterol-fed rabbits.View full abstractDownload PDF (1395K) -
Masafumi FUJIMOTO, Tadashi OKABAYASHI1986 Volume 41 Issue 2 Pages 223-227
Published: 1986
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe relationship between bradykinin (BK)-induced prostaglandin E2 (PGE2) and cyclic AMP syntheses in mouse fibrosarcoma cells (HSDM1C1) was investigated. Maximal BK-induced increases in cyclic AMP preceded increases in PGE2 production. PGE2 synthesis reached maximum at a much lower concentration of BK than cyclic AMP synthesis. Indomethacin completely inhibited BK-induced PGE2 production, but did not influence the cyclic AMP levels. Arachidonic acid in the medium induced PGE2 production in large quantities, but increased cyclic AMP accumulation only slightly. A high PGE2 concentration increased cyclic AMP levels only slightly. Theophylline increased basal and BK-mediated cyclic AMP levels, but did not affect PGE2 production at all. These results indicate that BK-evoked PGE2 and cyclic AMP syntheses in HSDM1C1 are not dependent upon each other.View full abstractDownload PDF (351K) -
Tsutomu OKIMURA, Masami OGAWA, Toshihiko YAMAUCHI1986 Volume 41 Issue 2 Pages 229-235
Published: 1986
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSSeveral experiments were conducted to evaluate the influences of restraint stress on cell-mediated immune events in mice. Delayed type hypersensitivity response to sheep red blood cells was inhibited by the stress, regardless of the timing of restraint stress loading. The activity of phagocytosis of macrophages in vitro and in vivo were measured by using the zymosan-particle uptake method and the carbon clearance test, respectively. Both activities were decreased in restraint-stressed mice. The suppressed carbon clearance rate in stressed mice, however, was recovered by the transfusion of serum from normal mice. Natural killer activity in spleen cells was decreased to 30-50% of the control in stressed mice. However, no suppressor cells which could inhibit NK activity existed in the spleen from stressed mice. These results show that the restraint stress suppresses various kinds of cell-mediated immune events, which might play an important role in anti-tumor immunity.View full abstractDownload PDF (487K) -
Tsutomu OKIMURA, Masami OGAWA, Toshihiko YAMAUCHI, Yasuo SASAKI1986 Volume 41 Issue 2 Pages 237-245
Published: 1986
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSWe investigated the correlation between restraint stress-induced alteration of antibody responses and adrenal hormones. Adrenalectomy (Adx) blocked both the suppression of antibody response against T cell-dependent (TD) antigen and the enhancement of that against T cell-independent (TI) antigen in stressed mice. Adx also inhibited the atrophy of both thymus and spleen caused by restraint. Pre-treatment of metyrapone, an inhibitor of adrenocortical steroid biosynthesis, had an effect that was similar to, but far weaker than that of Adx on stressed mice. The pre-administration of phenoxybenzamine, an α-adrenergic blocking agent, to mice prevented both the inhibition of antibody response to TD antigen and the decrease in spleen cell number of restrained mice. A similar effect was observed in mice pre-treated with 6-hydroxydopamine, an adrenergic neuron degenerating agent. However, no effects of these two agents were observed on the enhancement of antibody response to TI antigen. The suppressive effect of the antibody response to TD antigen was augmented by the pre-administration of propranolol, a β-adrenergic blocking agent. These results suggest that the suppression of the function of T cells in restrained mice are attributed to the released adrenocortical and adrenal medullary hormones and activated sympathetic nervous system and that the enhancement of B cell function is due to the adrenocortical hormones.View full abstractDownload PDF (609K) -
Hiroko NOMURA, Ken IZUHARA, Takahide NOMURA, Mitsushi KODAMA, Nobuki S ...1986 Volume 41 Issue 2 Pages 247-256
Published: 1986
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe interaction between α- and β-adrenergic agonists was examined with respect to amylase release from rat parotid glands. The effect of hypothyroid status on this interaction was also compared with that in euthyroid rats. Both methoxamine and clonidine potentiated isoproterenol-induced amylase release from parotid glands of eu- and hypothyroid rats, but the α2-adrenoceptor-mediated response disappeared in the hypothyroid rats. Dibutyryl cyclic AMP, a second messenger of β-adrenergic agonists, also showed essentially the same results as those of isoproterenol, but potentiation of dibutyryl cyclic AMP-induced amylase release with α-adrenergic agonists was mediated through only α1-adrenoceptors in both groups. Calcium ion plays an important role in the interaction between α- and β-adrenergic agonists. These results suggest that the potentiating effect of α-adrenergic agonists may be mediated at least in part through an unknown mechanism at the step distal to cyclic AMP formation in both eu and hypothyroid rats.View full abstractDownload PDF (736K) -
Piero DEL SOLDATO1986 Volume 41 Issue 2 Pages 257-259
Published: 1986
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe dual effects of clonidine on gastric experimental damage have been studied in the rat. At lower doses, clonidine prevents gastric lesions induced by oxotremorine plus neostigmine, probably through an α2-agonist mechanism; at higher doses, the compound potentiates dimaprit-induced gastric damage, probably through an H2-agonist mechanism.View full abstractDownload PDF (160K) -
Mikio ITO, Tamio TSUKAHARA, Yoshio SUZUKI1986 Volume 41 Issue 2 Pages 260-262
Published: 1986
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe effect of cimetidine on ulcer healing was investigated in rats with acetic acid induced ulcer who were permitted to intake food only between 9:30-10:30 a.m. and 6:00-7:00 p.m. When evaluated on the 15th and 21st days after operation, cimetidine (100 mg/kg × 2/day, p.o.) markedly decreased the ulcer index and the defective area of the ulcerated region. Moreover, this agent pronouncedly increased the decreasing index of exposed ulcer floor and the mucosal regeneration index. On the 21st day, the thickness of the ulcer base was decreased by this agent, the involution of granulation being indicated. Thus, marked healing-promoting action of cimetidine on acetic acid-induced ulcer was observed by limiting the food-intaking-time.View full abstractDownload PDF (203K) -
Masayasu KIMURA, Ikuko KIMURA, Masashi MUROI, Tomoko NAKAMURA, Shoji S ...1986 Volume 41 Issue 2 Pages 263-265
Published: 1986
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSGlycyrrhizin (GLR) and its newly synthesized derivatives, deoxoglycyrrhetol dihemisuccinate (I), deoxoglycyrrhetol dihemiphthalate (II), and the related compounds, carbenoxolone and glycyrrhetinic acid hemiphthalate (III), were assayed with or without paeoniflorin (PF) in mice diaphragm muscles. GLR-derivatives per se blocked the nerve-stimulated twitch tensions with the following order of potencies: carbenoxolone=III>II=I>GLR. The potencies paralleled the extent of muscle depolarization except in the case of I. GLR and I only increased muscle conductance. The blocking effects by GLR-derivat!ves per se on twitch responses are, therefore, can be explained by depolarization of muscle membranes and not by membrane conductance change. When carbenoxolone, II or GLR were blended with PF, the potentiation of the blocking effects observed may be related to the muscle depolarization rather than by the increase in membrane conductance.View full abstractDownload PDF (227K)
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