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Volume 64 (1994)
- Issue 4 Pages 229-
- Issue 3 Pages 135-
- Issue 2 Pages 65-
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Volume 64, Issue 3
Displaying 1-15 of 15 articles from this issue
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Mohammed M. Al-Harbi, Shoeb Qureshi, Mohammad M. Ahmed, Mohammad Raza, ...1994 Volume 64 Issue 3 Pages 135-139
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSSantonin, a sesquiterpene lactone, commonly found in the plants of the family Compositae was found to show significant antiinflammatory activity on acute inflammatory processes. The activity profile of santonin closely resembled that of a standard non-steroidal antiinflammatory drug, diclofenac sodium. It also showed a significant inhibitory effect on granuloma formation; however, this effect of santonin was less pronounced as compared to diclofenac sodium. Santonin caused a significant antipyretic effect in mice, which was found to be independent of the route of administration of the drug. It also increased the hot plate reaction time of treated mice, similar to morphine.View full abstractDownload PDF (324K) -
Tohru Masukawa, Kunio Nakanishi1994 Volume 64 Issue 3 Pages 141-146
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSDiethyldithiocarbamate (DEDC, 0.25-2.00 mmol/kg) injected into mice at 0.5 hr prior to alloxan administration dose-dependently protected the mice against the diabetogenic actions of 75 mg/kg alloxan. Disulfiram (DS, 0.50-2.00 mmol/kg), a corresponding disulfide form, also exhibited similar protection. The maximum effect of DEDC was found by dosing at 0.5 hr prior to alloxan, and the effect afforded by DEDC pretreatment persisted up to 3 hr, whereas the effect of DS was exhibited when the compound was given 0.5 hr prior to alloxan. Of the metabolites of DEDC, diethylamine and carbon disulfide had no effect. At 0.5 hr after injection, DEDC alone had a potent increasing ability on blood glucose in a dose-dependent manner, but DS was less potent. Mannoheptulose, an antagonist of glucose action at pancreatic β-cells, when given 24 min after DEDC and 6 min before alloxan, eliminated the DEDC-induced protection. Fasted mice did not exhibit hyperglycemia at 0.5 hr after DEDC injection, and alloxan given at that time produced diabetes. These findings indicate that DEDC itself protected mice from alloxan-induced diabetes by the indirect mechanism of producing hyperglycemia at the time of alloxan administration. The anti-diabetogenic action of low doses of DS and DEDC, in animals lacking hyperglycemia at the time of alloxan injection, is likely based on a mechanism other than one involving hyperglycemia.View full abstractDownload PDF (368K) -
Noriaki Maeda, Nobuya Matsuoka, Mayako Yamazaki, Hiroyuki Arakawa, Yos ...1994 Volume 64 Issue 3 Pages 147-153
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSStarting from the hypothesis that drugs which specifically activate the hippocampal cholinergic nerve activity may ameliorate memory impairments, we carried out a series of evaluations for a novel cognitive enhancer using enhancement of penile erection as a sign of cholinergic activation, and found FR64822. The compound facilitated penile erection in naive rats, and it ameliorated scopolamine-induced amnesia of rats in passive avoidance tasks with bell-shaped dose-response curves, while it dose-dependently reduced body weight gain in Zucker fatty rats. Pretreatment with sulpiride (32 mg/kg, p.o.) hardly affected the former two activities, but significantly reduced the anorectic activity in Zucker rats. Further evaluation of FR64822 derivatives characterized a second compound, FR121196, which induces penile erection and memory enhancement, but not body weight reduction. Memory enhancing and erection stimulating activities of FR121196 were abolished in rats treated with either cysteamine (200 mg/kg, s.c.), a somatostatin depletor, or lesioning of the serotonergic raphe nuclei. Thus, classic whole animal studies based on a hypothesis proved to be efficient for reaching our objective, the discovery of a new drug. They also gave us insight into the common somatostatinergic and serotonergic mechanisms underlying penile erection and memory improvement.View full abstractDownload PDF (528K) -
Tomio Morohashi, Tsuneyoshi Sano, Shoji Yamada1994 Volume 64 Issue 3 Pages 155-162
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSStrontium at low doses has been used to treat osteoporosis. However, excessive doses can disturb calcium metabolism. The aim of the present study was to determine a dose that does not have any significant toxic effects on calcium contents in bone and calcium metabolism, and, consequently, to distinguish between pharmacological and toxic doses in rats. The rats were divided into a control, 0.05%-Sr, 0.10%-Sr and 0.50%-Sr groups (strontium intake approx. 0, 87.5, 175 and 875 μcmol/day, respectively). All of the rats were pair-fed their respective diets containing various doses of strontium in single metabolic cages from when they were 36 to 63 days old. When the rats were 60 days old, bone formation, bone resorp tion, calcium balance and intestinal calcium absorption were calculated as calcium metabolic parameters over a 3-day period using calcium balance and kinetic studies. At the age of 64 days, the rats were sacrificed under anesthesia, and the femur and blood were collected. Calcium and strontium levels in the bone and serum were then measured. In the strontium groups that received less than 175 μmol/day, none of the calcium metabolic parameters were significantly affected. However, the calcium contents in the bone were significantly increased in the group that received 87.5 μmol/day group. On the other hand, in the group that received the highest dose of strontium (875 μmol/day), all of the calcium metabolic parameters measured were markedly suppressed. A decrease in calcium level in both the bone and serum was also observed. These results suggest that strontium at doses of less than 175 μmol per day does not have a toxic effect on calcium contents in bone or calcium metabolism in rats, and a dose of 87.5 μmol/day may be adopted for future evaluations of the efficacy of strontium in various experimental skeletal diseases.View full abstractDownload PDF (484K) -
Toshirou Kouno, Toru Egashira, Fusako Takayama, Yoshikuni Kudo, Yasumi ...1994 Volume 64 Issue 3 Pages 163-169
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSThe effects of methylprednisolone succinate (MP) on plasma lipid peroxidation, plasma SOD activity and superoxide production in polymorphonuclear leukocytes (PMNs) induced by lipopolysaccharide (LPS) were examined in rats in vivo and in vitro. In rats subjected to LPS treatment, plasma phosphatidylcholine hydroperoxide (PCOOH) levels significantly increased, and the plasma Cu, Zn-SOD activity decreased by about 75%. When rats were given 30 mg/kg of MP intravenously, MP suppressed the elevation of plasma PCOOH levels and partially inhibited the decrease in plasma Cu, Zn-SOD activity. MP also suppressed PMA-induced superoxide production in PMNs primed by LPS. In in vitro experiments, low concentrations of MP had no effect on NADPH-dependent lipid peroxidation, but 4 mM MP produced 50% inhibition. MP had little effect on PMA-induced superoxide production in PMNs primed by LPS. Moreover, MP had no radical-trapping effect on superoxide, hydroxyl radical and stable DPPH radical. These results suggest that the suppressive effect of plasma lipid peroxidation by MP is not due to radical-trapping effects or preventive anti-oxidation, but may involve the suppression of the lipid chain reaction in liver membrane resulting from PMA-induced superoxide anions generated by PMNs.View full abstractDownload PDF (482K) -
Koji Nishizawa, Osamu Inoue, Yuji Saito, Akira Suzuki1994 Volume 64 Issue 3 Pages 171-177
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSThe protective effects of Kamikihi-To (KMK), a traditional Chinese medicine, against cerebral ischemia, hypoxia and anoxia were investigated with various experimental models in mice and gerbils. KMK (2.0 g/kg/day, p.o. for 5 days) significantly prolonged the survival time of mice subjected to bilateral common carotid artery occlusion. KMK (0.5 and 2.0 g/kg/day, p.o. for 5 days) also prolonged the survival time of mice injected with N-methyl-D-aspartic acid (NMDA: 80 mg/kg, i.v.). Furthermore, KMK (in a diet containing 8% KMK given orally for 34 days) showed protective effects against delayed neuronal death in CA1 pyramidal cells in the gerbil hippocampus after transient forebrain ischemia. On the other hand, we failed to show any protective effects of KMK (0.5-2.0 g/kg/day, p.o. for 5 days) against normobaric hypoxia and KCN-induced cytotoxic anoxia in mice. These results suggest that KMK may have protective effects against cerebral ischemic disorders, but not against severe hypoxic and anoxic disorders.View full abstractDownload PDF (633K) -
Masaki Ozawa, Yukie Nakada, Keiko Sugimachi, Fumie Yabuuchi, Tetsuo Ak ...1994 Volume 64 Issue 3 Pages 179-187
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSβ-Carboline abecarnil was behaviorally and biochemically characterized as a new anxiolytic agent in rodents and primates in comparison with the benzodiazepine (BZ) anxiolytics. Oral treatment with abecarnil (0.5-10 mg/kg) showed a potent anticonflict activity in the water-lick test in rats. The minimal effective dose was lower than those of BZ anxiolytics, such as etizolam, diazepam, clotiazepam and tofisopam. Abecarnil also showed taming effects to suppress fighting and aggressive behaviors in mice and monkeys with little sedative and ataxic effects, in contrast to the BZ anxiolytics producing marked sedative and ataxic effects. Furthermore, abecarnil suppressed both the sedative and ataxic effects induced by diazepam. Abecarnil bound to rat cerebellar BZ1 receptors (Ki=0.24 nM) with a higher affinity than to rat spinal cord BZ2 receptors (Ki=1.3 nM), whereas BZ derivatives bound to both the receptors with a low and equal affinity. GABA-ratios of abecarnil were 1.9 for the BZ1 receptors and 2.8 for the BZ2 receptors, and they were smaller than those of diazepam and flunitrazepam. Thus, in contrast to the BZ derivatives, abecarnil may act as a selective partial agonist at central BZ1 receptors, resulting in its potent anticonflict and taming effects with little sedative and ataxic effects.View full abstractDownload PDF (618K) -
Hajime Nakanishi, Kiyotaka Katsuta, Takako Koide, Yoshiko Ueda, Kiyoha ...1994 Volume 64 Issue 3 Pages 189-193
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSExcitatory amino acids and their receptors have been postulated to be involved in mediating ischemic neuronal damage. We occluded the bilateral carotid arteries for 5 min in gerbils to examine the effect of FR115427, a novel N-methyl-D-aspartate (NMDA) antagonist, on ischemic neuronal damage. FR115427 prevented hippocampal CA1 cell damage at a dose of 10 mg/kg and reduced spontaneous locomotor hyperactivity in gerbils after the development of ischemia at a dose of 32 mg/kg. The effective doses of MK801 were 3.2 mg/kg for preventing hippocampal CA1 cell damage and 1 mg/kg for reducing spontaneous locomotor hyperactivity. Moreover, we monitored the changes in body temperature of ischemic gerbils for 24 hr. The body temperature of ischemic gerbils significantly increased 1 hr after reperfusion. The pretreatment with FR115427 or MK801 prevented the hyperthermia provoked 1 hr after reperfusion in ischemic gerbils. In addition, the hypothermia was developed in gerbils treated with MK801 24 hr after reperfusion. However, FR115427 did not show hypothermia at any time. These results indicate that FR115427 has a protective effect against ischemic hippocampal CA1 cell damage after systemic administration, and this protective effect appears to be due to anti-NMDA activity.View full abstractDownload PDF (417K) -
Ikuko Kimura, Youichi Nakano, Takeshi Naitoh, Motonori Okabe, Masayasu ...1994 Volume 64 Issue 3 Pages 195-200
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSWe investigated the effect of diabetic plasma on insulin-stimulated DNA synthesis in primary cultured aortic smooth muscle cells (SMC) of the GK rat, a model of non-insulin-dependent diabetes mellitus, and compared it with that of Wistar normal rat plasma. We measured the incorporation of 3H-thymidine into cultured SMC. The diabetic plasma (3%) of GK rat, but neither the plasma (3%) of Wistar normal rat nor the plasma (3%) (not containing both insulin-like growth factor-I (IGF-I) and corticosterone) of Wistar hypophysectomized rat induced insulin-stimulated DNA synthesis in GK rat SMC. The responsiveness of SMC to insulin, not to IGF-I, was decreased remarkably by the diabetic state. The diabetic plasma of GK rat remarkably enhanced and the plasma of Wistar hypophysectomized rat weakly enhanced insulin-stimulated DNA synthesis in Wistar normal rat SMC. Corticosterone (20 nM) increased insulin-stimulated DNA synthesis in GK rat SMC but decreased it in Wistar normal rat SMC, using the plasma of Wistar hypophysectomized rat. Corticosterone levels were lower in GK rat plasma than in normal Wistar rat plasma. These results demonstrate that the enhancement of insulin-stimulated DNA synthesis in diabetic SMC by the diabetic plasma of GK rat may be due to neither IGF-I nor corticosterone but due to other factors.View full abstractDownload PDF (451K) -
Hiromi Tsushima, Seigo Fujimoto, Tomohiro Matsuda1994 Volume 64 Issue 3 Pages 201-207
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSWe investigated effects of β-adrenoceptor agonists (β1-selective: T-1583 and dobutamine, β2-selective: fenoterol, non-selective: isoproterenol) on urine outflow rate, blood pressure, heart rate, respiratory rate and rectal temperature. The drugs were applied into the paraventricular nuclei (PVN) of spontaneously hypertensive (SHR), Wistar-Kyoto (WKY) and Wistar rats. Fenoterol and isoproterenol markedly decreased the urine outflow rate, compared with T-1583 and dobutamine in the rats. There was no marked difference among the three strains in responsiveness to fenoterol and isoproterenol. The antidiuretic effects of fenoterol were inhibited by a β2-selective antagonist, butoxamine, more markedly than β1-selective antagonist, atenolol, in SHR; and the inhibitory effects of these drugs were partial in WKY. In Wistar rats, the effect of fenoterol was inhibited by a non-selective β-antagonist, timolol, but not by atenolol or butoxamine. A vasopressin antagonist (i.v.) did not diminish the antidiuretic effect of fenoterol. Fenoterol reduced the blood pressure in SHR and WKY, but not in Wistar rats. It was suggested that there were predominantly β2-adrenoceptors mediating antidiuresis in SHR. In WKY and Wistar rats, however, the β-adrenoceptor subtypes mediating antidiuresis have yet to be determined. The ability of β-adrenoceptor agonists to decrease urine outflow rates in SHR was not altered as compared to that in the control rats. β-Adrenoceptor-mediated antidiuresis was not due to vasopressin release.View full abstractDownload PDF (487K) -
Seiji Ichida, Tetsuyuki Wada, Naruhisa Matsuda, Satori Nakazaki1994 Volume 64 Issue 3 Pages 209-212
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSWe investigated the effects of various Ca channel agonists (Ca agonist) derived from 1, 4-dihydropyridine on KCl-stimulated 45Ca uptake by differentiated and undifferentiated neuroblastoma × glioma hybrid NG108-15 cells with and without dibutyryl cAMP. Ca agonists Bay K 8644, YC-170 and CGP 28392 enhanced KCl-stimulated 45Ca uptake in differentiated NG108-15 cells, but only slightly in undifferentiated NG108-15 cells. The rank order of the enhancing effects was roughly Bay K 8644 > YC-170 >> CGP 28392. These results suggest that there is some difference between the mechanisms by which these Ca agonists affect KCl-stimulated 45Ca uptake in differentiated and undifferentiated NG108-15 cells, although the nature of that difference is not clear.View full abstractDownload PDF (221K) -
Nagao Suzuki, Ken Mizuno, Yasuo Gomi1994 Volume 64 Issue 3 Pages 213-216
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSIn guinea pig ileal circular muscle, electrical stimulations by a train of 10-100 pulses (0.05-msec duration, 10 Hz) produced tetrodotoxin-sensitive "off" contractions that were initiated upon the termination of stimulations. Atropine at 10-6M did not inhibit the "off" contractions. FK224 at 10-5M, a dual antagonist for NK1 and NK2-receptors, but not 10-7M CP-96, 345, an antagonist for NK1-receptors, almost abolished the "off" contractions in the presence of atropine. These results suggest that the neurogenic "off" contraction was mediated mainly by NK2-receptors in the circular muscle of guinea pig ileum.View full abstractDownload PDF (305K) -
Minoru Isosaki, Naoki Minami, Toshikatsu Nakashima1994 Volume 64 Issue 3 Pages 217-219
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSCalphostin C, a protein kinase C inhibitor, reduced phorbol ester-induced enhancement of catecholamine secretion but not primary Ca2+-induced secretion from digitonin-permeabilized bovine adrenal medullary cells, indicating that this compound selectively inhibited protein kinase C-dependent secretion.View full abstractDownload PDF (192K) -
Yasuo Morimoto, Koichi Shimohara, Keiko Tanaka, Hideaki Hara, Takayuki ...1994 Volume 64 Issue 3 Pages 221-224
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSBoth KB-5492, a new anti-ulcer agent, and cimetidine, administered orally at 25-200 mg/kg, dose-dependently prevented cysteamine (400 mg/kg, s.c.)-induced duodenal ulcers in rats with ED50 values of 63 and 40 mg/kg, respectively. Anti-ulcer doses of cimetidine, but not KB-5492, inhibited gastric acid hypersecretion induced by cysteamine (400 mg/kg, s.c.). In contrast, anti-ulcer doses of KB-5492, but not cimetidine, increased duodenal HCO3- secretion in normal anesthetized rats. These findings suggest that KB-5492 prevents cysteamine-induced duodenal ulcers by stimulating duodenal HCO3- secretion, whereas cimetidine does so by inhibiting cysteamine-induced gastric acid hypersecretion.View full abstractDownload PDF (250K) -
Yuji Ikegaya, Hiroshi Saito, Norio Matsuki1994 Volume 64 Issue 3 Pages 225-227
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSTo elucidate the role of carbon monoxide (CO) in hippocampal long-term potentiation (LTP), the effect of an inhibitor of heme oxygenase, which produces carbon monoxide, was investigated in the dentate gyrus of anesthetized rats. Administration of zinc protoporphyrin IX (100 nmol, i.c.v.) 30 min before the tetanic stimulation of 30 pulses at 60 Hz attenuated the intensity of LTP. However, this drug did not affect the established LTP. These results suggest that CO participates in the generation of LTP in vivo.View full abstractDownload PDF (164K)
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