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Volume 35 (1984)
- Issue 4 Pages 339-
- Issue 3 Pages 203-
- Issue 2 Pages 79-
- Issue 1 Pages 1-
Volume 35, Issue 2
Displaying 1-16 of 16 articles from this issue
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B. MARTINEZ, E.J. STABA1984 Volume 35 Issue 2 Pages 79-85
Published: June 01, 1984
Released on J-STAGE: March 23, 2011
JOURNAL FREE ACCESSRelative and total amount of saponins in Panax ginseng, Panax quinquefolius, Aralia mandshurica and Eleutherococcus senticosus were determined by thin-layer chromatography and by a spectrophotometric method. The ginsenoside Rg1 was present in American ginseng. Aralia and Eleutherococcus did not contain diol- and triol-type ginsenosides. Low concentrations of ginsenosides were found in Oriental red ginsengs (1.4-2.7%). Orally administered Araliaceae saponin extracts did not affect plasma lactic acid, glucagon, insulin or liver glycogen levels in exercised rats and did not prolong their swimming time. Plasma glucose levels in resting rats were decreased by saponin extracts of Canadian white, American red, Sanchi, Aralia, Eleutherococcus, Korean red and Shiu-Chi ginsengs.View full abstractDownload PDF (1002K) -
Norihisa INAZU, Hiroshi KOGO, Yoshio AIZAWA1984 Volume 35 Issue 2 Pages 87-93
Published: June 01, 1984
Released on J-STAGE: March 23, 2011
JOURNAL FREE ACCESSIn order to examine a possible role of the pituitary gland and uterine tissue in the formation of 13, 14-dihydroprostaglandin F2α (13, 14H2-PGF2α) in rat ovary, hypophysectomized and hysterectomized rats were used. Gonadotropins stimulated the formation of 13, 14H22-PGF2α from prostaglandin F2α (PGF2α) and 13, 14-dihydro-15-keto-PGF2α (15KD-PGF2α) in the ovarian homogenate of hypophysectomized and hysterectomized rats as well as in intact rats. Ovarian steroids, estradiol and progesterone, reduced the formation of 13, 14H2-PG F2α in the ovarian homogenate of intact rats. However, in hysterectomized and hypophysectomized rats, its formation was not affected by ovarian steroids. On the other hand, when pregnant mare serum gonadotropin (PMS) and estradiol were simultaneously administered to intact and hypophysectomized rats, the formation of 13, 14H2-PG F2α in the ovary showed a tendency to be increased as compared with that after treatment with PMS alone. These results not only suggest that the formation of 13, 14H2-PGF2α, in rat ovary is regulated by gonadotropins and ovarian steroids, but also that uterine tissue may take part in the process of its formation.View full abstractDownload PDF (1219K) -
Shigeru OKUYAMA, Hironaka AIHARA1984 Volume 35 Issue 2 Pages 95-103
Published: June 01, 1984
Released on J-STAGE: March 23, 2011
JOURNAL FREE ACCESSThe analgesic activities of intracerebroventricular (icy) administrations of some analgesic drugs, morphine, indomethacin, diclofenac, aminopyrine and acetaminophen, were studied in comparison with those of systemic administrations in normal rats and adjuvant arthritic rats. A method for the measurement of analgesic potency in normal rats and adjuvant arthritic rats were developed using the vocalization response as an indicator of pain resulting from electrical stimulation. The systemic and/or icy administered indomethacin and diclofenac produced much more potent analgesic action in adjuvant arthritic rats than in normal rats. Morphine, aminopyrine and acetaminophen given by the two routes showed roughly the same analgesic effect in both types of rats. Simultaneous systemic and icy administrations of indomethacin and/or diclofenac showed an additive effect in normal rats, but showed a synergistic effect rather than a simple additive effect in adjuvant arthritic rats. Those of morphine, aminopyrine and acetaminophen showed only additive effects in both types, except for that of aminopyrine in normal rats. Moreover, the brain and serum levels of non-metabolized indomethacin and aminopyrine were measured after the normal and adjuvant arthritic rats were systemically given these drugs. In adjuvant arthritic rats, the icy effective dose of indomethacin was the same as the brain level of non-metabolized indomethacin after the systemic administration. The effective dose of indomethacin administered icy in the normal rats was 17 times higher than the brain level of non-metabolized indomethacin administered systemically. The icy effective dose of aminopyrine was 4-4.5 times higher than the level of the brain concentration of non-metabolized drug in both types of rats. It was suggested that acidic nonsteroidal antiinflammatory drugs (NSAIDs) such as indomethacin and diclofenac specifically inhibit inflammatory pain, and the pain-relieving properties of acidic NSAIDs may be related to the central as well as the peripheral site of action.View full abstractDownload PDF (2531K) -
Morihiko YOSHINO, Toshio OBATA, Sadayuki SHO, Hiroyasu KINEMUCHI1984 Volume 35 Issue 2 Pages 105-115
Published: June 01, 1984
Released on J-STAGE: March 23, 2011
JOURNAL FREE ACCESSThe present study was undertaken to clarify the enzymic and molecular properties of monoamine oxidase (MAO) in carp brain. In particular, its sensitivities to selective MAO inhibitors, kinetic properties and molecular weight were compared with those of the enzyme in carp liver. The selective and potent MAO-A and MAO-B inhibitors FLA 788 (+), FLA 336 (+), MD 780236 and benzylcyanide caused dose-dependent inhibitions of MAO activity in both carp brain and liver; the inhibition curves were all single-sigmoidal, and the degrees of inhibition of the activities towards 5- hydroxytryptamine (5-HT, selective MAO-A substrate), tyramine (substrate for both forms of MAO) and β-phenylethylamine (PEA, selective MAO-B substrate) were similar. This was also the case for inhibition of activity in carp brain by the irreversible and selective MAO-A and MAO-B inhibitors clorgyline and I-deprenyl, indicating the presence in both preparations of a single MAO which differs from either form of MAO. Studies on the substrate specificities and Km values for these three substrates and the inhibitory effects of some compounds suggested that the enzymic characters of MAO in carp preparations were similar and that these enzymes might be FAD-containing enzymes, like MAO in various mammals. By labelling the preparations with radioactive pargyline and then subjecting them to sodium dodecyl sulfate electrophoresis, the apparent molecular weights of carp brain and liver MAO were estimated as 60, 000 daltons. The same value was also obtained for rat brain and liver mitochondrial MAO-B. These results indicate that by the present definitions of MAO-A and MAO-B, MAO in carp brain and liver is similar to, but distinct from, both these forms of MAO.View full abstractDownload PDF (1764K) -
Huei-Yann TSAI1984 Volume 35 Issue 2 Pages 117-121
Published: June 01, 1984
Released on J-STAGE: March 23, 2011
JOURNAL FREE ACCESSThe relationship between neuropeptides and serotonergic neurones was investigated in rat spinal cord, in vivo, using a subarachnoidal perfusion technique. The 5-hydroxytryptamine (5-HT) release from the spinal cord could be evoked by substance P and peripheral pain stimulation (tail pinch), but not by methionine-enkephalin (met-EK). The substance P-evoked 5-HT release was slightly potentiated by met-EK. The tail pinch-evoked 5-HT release was inhibited by met-EK and baclofen, but potentiated by naloxone. These findings may infer a possible mechanism by which neuroactive peptides regulate 5-HT release from serotonergic neurones in the spinal cord.View full abstractDownload PDF (666K) -
Hisashi KURIBARA, Akihiro HIGASHIDA, Sakutaro TADOKORO1984 Volume 35 Issue 2 Pages 123-128
Published: June 01, 1984
Released on J-STAGE: March 23, 2011
JOURNAL FREE ACCESSEffects of disulfiram and calcium cyanamide, antialcoholic drugs, on schedule-induced ethanol drinking as well as on schedule-controlled response (lever-pressing) under a fixed interval 1 min schedule of food reinforcement were investigated in Wistar strain rats. When ethanol solution was available, the schedule-induced ethanol drinking decreased depending on the ethanol concentration (2-8%). However, the dose of ethanol intake during the 1 hr experimental session was at maximum (2.8 g/kg) when 4% ethanol solution was available. Thereafter, 4% ethanol solution was used in the experiment for studying the effects of disulfiram and calcium cyanamide on the schedule-induced ethanol drinking. Disulfiram (100-200 mg/kg, p.o.), pretreated at 1 hr before the start of the experiment, tended to suppress schedule-induced water drinking. However, the same treatment of calcium cyanamide (5-10 mg/kg, p.o.) did not produce a marked change in it. In contrast, disulfiram (100 and 200 mg/kg) and calcium cyanamide (5 and 10 mg/ kg) markedly suppressed schedule-induced ethanol drinking without eliciting a marked change in schedule-controlled response. The present results suggest that both disulfiram and calcium cyanamide selectively suppress ethanol drinking in rats.View full abstractDownload PDF (1084K) -
I. A Biochemical and Histological Study of the Effects of Pretreatment with Cadmium on the Acute Oral Toxicity of Cadmium in MiceShigeru MORITA1984 Volume 35 Issue 2 Pages 129-141
Published: June 01, 1984
Released on J-STAGE: March 23, 2011
JOURNAL FREE ACCESSResistance to the lethal action of Cd2+ produced in mice was maintained for 6 to 24 hr after pretreatment with 1/10 of the challenge Cd2+ doses as shown by an increased oral LD50. Pretreatment 24 hr prior to the challenge doses was most effective. In addition, 1/20 to 1/7 of the challenge doses was necessary to acquire the tolerance to the acute oral toxicity of Cd2+. The largest effect was found for pretreatment with 1/7 of the challenge doses. Acute liver injury at 24 hr after challenge with a large dose of Cd2+ (100 mg Cd2+/kg, p.o.) was markedly reduced by pretreatment with a small dose of the cation (15 mg Cd2+/kg, p.o.) 24 or 48 hr prior to the challenge dose as shown by a marked reduction in serum GOT and GPT activities and the reversal of histopathological changes. The elevated serum urea nitrogen at 4 hr after the Cd2+ challenge was reduced by pretreatment 6 to 24 hr prior to the challenge dose. In spite of the increased urea nitrogen 4 hr after the Cd2+ challenge, no morphological alterations were observed in the kidney at 24 hr. Serum Alp activity was not significantly influenced by the Cd2+ challenge. Glucose in serum was increased by the administration of a small dose of Cd2+, but was unaffected by a large dose. Decreases in hepatic RNA and DNA concentrations at 24 hr after the Cd2+ challenge were prevented by pretreatment 24 or 48 hr prior to the challenge dose. Potentiation of hexobarbital sleep time was observed at 6 or 24 hr after a small dose of Cd2+. Nevertheless, further potentiation at 24 hr after the Cd2+ challenge (75 mg Cd2+/kg, p.o., in this case) was reduced by pretreatment 24 hr prior to the challenge dose. A major target organ for the acute oral toxicity of Cd2+ was the liver rather than the kidney.View full abstractDownload PDF (4717K) -
II. Effects of Pretreatment with a Small Oral Dose of Cadmium on Absorption, Distribution and Excretion of Cadmium after a Large Oral Dose in MiceShigeru MORITA1984 Volume 35 Issue 2 Pages 143-151
Published: June 01, 1984
Released on J-STAGE: March 23, 2011
JOURNAL FREE ACCESSUptake of Cd2+ by the liver and kidney of female mice 24 hr after challenge with a large dose of Cd2+ (100 mg Cd2+/kg, p.o.) was greatly reduced by pretreatment with a small dose of the cation (15 mg Cd2+/kg, p.o.) at 24 hr (for liver) and at 6, 24 or 48 hr (for kidney) prior to the challenge dose. The hepatic concentration of Zn2+ tended to be increased by the Cd2+ challenge and was increased further by pretreatment. The renal concentration of Zn2+ was not influenced by Cd2+ administration. The retention rate of Cd2+ in the stomach and its contents 24 hr after the Cd2+ challenge was decreased by pretreatment. In addition, the excretion rate of Cd2+ into the feces 24 hr after the Cd2+ challenge was increased by pretreatment at 6 to 24 hr prior to the challenge dose. Consequently, the absorption rate of Cd2+ 24 hr after the Cd2+ challenge was markedly reduced by pretreatment at 24 hr prior to the challenge dose. The urinary and biliary excretion of Cd2+ was very low. The motility of the small intestine was stimulated 6 hr after a small dose of Cd2+, but returned to normal within 24 hr. The motility tended to be reduced 4 hr after the Cd2+ challenge, but conversely, it was facilitated at 24 hr. Pretreatment at 6 or 24 hr prior to the challenge dose prevented the reduction of the motility 4 hr after the Cd2+ challenge.View full abstractDownload PDF (1231K) -
III. Effects of Pretreatment with a Small Oral Dose of Cadmium on Metallothionein Synthesis after a Large Oral Dose of Cadmium in MiceShigeru MORITA1984 Volume 35 Issue 2 Pages 153-161
Published: June 01, 1984
Released on J-STAGE: March 23, 2011
JOURNAL FREE ACCESSPretreatment of female mice with a small oral dose of Cd2+ (15 mg Cd2+/kg) decreased Cd2+ uptake by the liver and kidney and increased that by the small intestinal mucosa at 4 or 24 hr after challenge with a large oral dose of Cd2+ (100 mg Cd2+/kg). By 4 hr after the challenge dose, more Cd2+ taken up by the liver was bound to metallothionein (MT) in the Cd2+-pretreated mice than the water-pretreated controls (10 ml H2O/kg); but at 24 hr, the amount of Cd2+ bound to MT in the liver and kidney were lower in the former than the latter. The amount of Cd2+ not bound to MT in the liver at 4 and 24 hr after the challenge dose and that in the kidney at 24 hr were lower in the Cd2+-pretreated mice than the water-pretreated controls. These results suggested that the factor directly related to the toxic action of Cd2+ was the amount of Cd2+ not associated with MT in the liver and other organs. More Cd2+ taken up by the small intestinal mucosa at 24 hr after the challenge dose was associated with MT in the Cd2+-pretreated mice than the water-pretreated controls. The present study indicates that MT induced in the small intestinal mucosa by pretreatment prevents Cd2+ absorption by sequestering subsequently administered Cd2+, and Cd2+ taken up by the liver and kidney is bound to MT in an inert form, thus the decrease in the amount of Cd2+ not bound to MT, giving protection from the acute oral toxicity of the cation. Pretreatment 24 hr prior to the challenge dose was found to be the most effective.View full abstractDownload PDF (1561K) -
Tamotsu NAKANO, Satoshi KAWAI, Toshiharu NAGATSU1984 Volume 35 Issue 2 Pages 163-167
Published: June 01, 1984
Released on J-STAGE: March 23, 2011
JOURNAL FREE ACCESSA new fluorometric assay for the determination of monoamine oxidase activity that is applicable to any substrates including dopamine and serotonin is described. Hydrogen peroxide formed during the monoamine oxidase reaction was reduced in the presence of glutathione and glutathione peroxidase, and the oxidized glutathione was measured fluorometrically as NADP+ via oxidation of NADPH by glutathione reductase. This method was applied for inhibitor studies using clorgyline and deprenyl.View full abstractDownload PDF (787K) -
Shinji SHIBANOKI, Yukinobu GOTOH, Koichi ISHIKAWA1984 Volume 35 Issue 2 Pages 169-174
Published: June 01, 1984
Released on J-STAGE: March 23, 2011
JOURNAL FREE ACCESSA simple and sensitive procedure was developed for determining the concentration of chlorpromazine (CPZ) in the blood and brain of mice with promethazine as the internal standard. The procedure involves (1) primary extraction by a mixture of heptane and isoamyl alcohol (99 : 1) in an alkaline condition and (2) determination by means of high performance liquid chromatography with electrochemical detection. The detection limit of CPZ was 0.5 ng for one chromatographic injection. The drug was detectable in a 100 μl sample of the blood by 6 hr after an intravenous injection of 0.25 mg/kg. The concentration of CPZ was about 40 times higher in the brain compared with that in the blood. The biological half life was estimated to be 87 and 65 min, in the blood and brain, respectively. The proposed method is also applicable for the determination of other phenothiazine derivatives and effective for pharmacokinetic study of the compounds in clinics and laboratories.View full abstractDownload PDF (953K) -
Masakatsu TAKAHASHI, Reiko IZUMI, Hiroshi KANETO1984 Volume 35 Issue 2 Pages 175-179
Published: June 01, 1984
Released on J-STAGE: March 23, 2011
JOURNAL FREE ACCESSInvolvement of the catecholaminergic mechanism in foot shock (FS) - and immobilized-water immersion (IW) -stress-induced analgesia (SIA) and in the development of tolerance to the effect were investigated in mice. With daily treatment with clonidine or daily exposure to stresses, tolerance developed rapidly to the analgesic effect. Clonidine-induced analgesia, which could not be antagonized by naloxone, was potentiated in the animals rendered tolerant to FS-stress, and it was attenuated in the animals tolerant to IW-SIA. On the other hand, animals tolerant to clonidine failed to show the attenuation of FS- and IW-SIA. The analgesic effect of clonidine and the development of tolerance to the effect were not influenced by reserpine. However, reserpine pretreatment completely suppressed the analgesic effect induced by FS- and IW-stresses on the 1st day; but with daily exposure to the stress, the analgesic effect gradually appeared and returned to the control level on the 5th day. These results indicate not only the differences between clonidine analgesia and SIAs but also those between each SIA. Thus, the central catecholaminergic mechanisms play an important role in these SIAs and also in the development of tolerance to the effect, although the degree of participation of these mechanisms seems to be somewhat different between FS- and IW-SIA, as indicated by the cross-tolerance between clonidine analgesia and each SIA.View full abstractDownload PDF (759K) -
Keiichi TANAKA, Keiko KANAOKA, Mihoko EGAWA, Norio ABE, Isao WATANABE, ...1984 Volume 35 Issue 2 Pages 181-191
Published: June 01, 1984
Released on J-STAGE: March 23, 2011
JOURNAL FREE ACCESSThe effect of piroxicam on polymorphonuclear neutrophils (PMN) functions induced by several stimuli was evaluated in vitro. Preincubation of rabbit or human PMN with piroxicam inhibited the cellular responses elicited by N-formyl-methionyl-leucyl-phenylalanine (FMLP) such as superoxide anion (O2-) generation, granule enzyme release and chemotaxis. The effectiveness of piroxicam on each response was superior to those of indomethacin and ibuprofen. Also when either concanavalin A, zymosan-treated serum or ionophore A23187 was used as stimuli, piroxicam inhibited O2- generation of PMN. The inhibitory effect of piroxicam on FM LP-induced O2- generation was dependent on the concentration of stimuli and was reversed, by increasing the extracellular calcium concentration. In addition, piroxicam had no effect on the activity of a chymotrypsin-like esterase, N-acetyl-phenylalanine-β-naphthyl esterase, isolated from rabbit PMN. These results suggest that at least some of the anti-inflammatory effects of piroxicam may be mediated by affecting PMN functions, and the inhibition of O2- generation of PMN by piroxicam may be related to its capacity to modulate the association of calcium with these cells.View full abstractDownload PDF (1873K) -
Chiaki KAMEI, Tatsuro DABASAKI, Kenji TASAKA1984 Volume 35 Issue 2 Pages 193-195
Published: June 01, 1984
Released on J-STAGE: March 23, 2011
JOURNAL FREE ACCESSDownload PDF (455K) -
Masahiro SUNO, Akinobu NAGAOKA1984 Volume 35 Issue 2 Pages 196-198
Published: June 01, 1984
Released on J-STAGE: March 23, 2011
JOURNAL FREE ACCESSDownload PDF (364K) -
Shigetoshi CHIBA, Miyoko TSUKADA1984 Volume 35 Issue 2 Pages 199-201
Published: June 01, 1984
Released on J-STAGE: March 23, 2011
JOURNAL FREE ACCESSDownload PDF (540K)
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