All issues
Successor
Volume 60 (1992)
- Issue 4 Pages 315-
- Issue 3 Pages 153-
- Issue 2 Pages 67-
- Issue 1 Pages 1-
Volume 60, Issue 2
Displaying 1-14 of 14 articles from this issue
- |<
- <
- 1
- >
- >|
-
Sadek A. Taha1992 Volume 60 Issue 2 Pages 67-71
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSThe compound ambrein was isolated from ambergris, which is commonly used as an analgesic in the Saudi folklore medicine. The LD50 of ambrein, given intraperitoneally (i.p.) in mice, was found to be high (7.5 g/kg), and ambrein proved to be a safe compound in this species. In the hotplate test, ambrein was found to possess antinociceptive activity in mice at doses which did not sedate or incapacitate the animals. By the i.p. administration route, ambrein produced antinociception in mice at a dose as low as 10 mg/kg. The antinociceptive activity of ambrein (250 mg/kg i.p.) was inhibited by a noradrenergic neurotoxin (DSP-4) and by naloxone, methysergide or prazosin. It was not influenced by a serotonin depletor, p-chlorophenylalanine. The possible mechanism of ambrein antinociception is discussed.View full abstractDownload PDF (304K) -
Kohtarou Kodama, Hideyuki Adachi, Toshiaki Ogawa, Hideto Ohhara1992 Volume 60 Issue 2 Pages 73-77
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSWe compared the antianginal effect of E4080, a novel bradycardic agent with coronary vasodilating properties, with those of a bradycardic agent and some coronary vasodilators in vasopressin-induced anginal model of guinea pigs. An i.v.-administration of vasopressin (0.2IU/kg) produced an ST segment elevation on electrocardiograms (ECG) of 0.30 ± 0.05 mV from the baseline within 30 sec in anesthetized guinea pigs. The ST segment elevation on ECG was used as an index of myocardial ischemia. E4080 and other drugs were injected i.v. 5 min before the administration of vasopressin. E4080 at 5 mg/kg depressed the ST segment elevation induced by vasopressin to 0.06 ± 0.01 mV (20% of control, n = 6, P < 0.001). However, alinidine (5 mg/kg), which produced the same bradycardic action (reduction of heart rate by 50%) as that of E4080, tended to inhibit the ST segment elevation, but this was not statistically significant. On the other hand, other vasodilators such as isosorbide dinitrate (0.3 mg/kg), nifedipine (0.1 mg/kg) and lemakalim (1 mg/kg) also significantly reduced the ST segment elevation to 0.16 ± 0.03, 0.08 ± 0.04 and 0.09 ± 0.03 mV, respectively. These results suggest that the inhibitory effect of E4080 on the ST segment elevation induced by vasopressin is due to the coronary vasodilating effect rather than the bradycardic effect, and that E4080 would be useful as an antianginal agent.View full abstractDownload PDF (348K) -
Kenji Tobetto, Tadashi Yasui, Takao Ando, Masahiro Hayaishi, Noriko Mo ...1992 Volume 60 Issue 2 Pages 79-84
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSThe effects of hyaluronan (HA) on the release of arachidonic acid (AA) from phospholipids induced by bradykinin in synovial fibroblasts of osteoarthritic patients were examined. HA inhibited [14C]AA release from prelabeled synovial cells stimulated with and without bradykinin 1 hr after incubation with HA and thereafter. The inhibitory effects of HA on [14C]AA release were dependent on the concentration and molecular weight of HA. However, inhibition of [14C]AA release by HA was not merely due to the viscosity of HA. The [14C]AA release induced by calcium-ionophore A23187 was also inhibited by HA with a high molecular weight. In addition, HA did not affect [14C]AA uptake by the cells. Our results suggest that HA with a high molecular weight elicits anti-inflammatory effects, at least in part, by inhibiting AA release in inflamed joints.View full abstractDownload PDF (378K) -
Haruo Suzawa, Shinji Kikuchi, Kiyoshi Ichikawa, Akihide Koda1992 Volume 60 Issue 2 Pages 85-90
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSTranilast, an anti-allergic drug that inhibits the release of substances such as histamine and prostaglandins from mast cells, has been reported to improve keloids and hypertrophic scars which originate from the abnormal proliferation and excessive collagen accumulation of fibroblasts. It has been considered that various chemical mediators produced by inflammatory cells play important roles in the development of keloids and hypertrophic scars. We therefore studied the effect of tranilast on the release of chemical mediators including transforming growth factor (TGF)-β1, interleukin (IL)-1β and prostaglandin (PG) E2 which are produced by the human monocytes-macrophages, and estimated whether these mediators induce collagen synthesis and cell proliferation of normal skin fibroblasts. Tranilast inhibited the release of TGF-β1, IL-1β and PGE2 from the human monocytes-macrophages. TGF-β1 (25-200 pM) enhanced the collagen synthesis by fibroblasts. IL-1 (0.1-1 U/ml) increased the proliferation and conversely decreased the collagen synthesis. PGE2 (2 μg/ml) enhanced the collagen synthesis. These results suggest that tranilast suppresses collagen synthesis by fibroblasts through inhibiting TGF-β1 and PGE2 production and cell proliferation by fibroblasts through inhibiting IL-1 production by inflammatory cells such as macrophages.View full abstractDownload PDF (400K) -
Haruo Suzawa, Shinji Kikuchi, Nobuhiko Arai, Akihide Koda1992 Volume 60 Issue 2 Pages 91-96
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSTranilast, an anti-allergic drug inhibiting the release of substances such as histamine and prostaglandins from mast cells, was previously reported to suppress collagen synthesis of fibroblasts derived from keloid tissues. However, the inhibitory mechanism on collagen synthesis is unknown. We studied its inhibitory mechanism on collagen synthesis by culturing fibroblasts from keloid and hypertrophic scar tissues of humans. Collagen synthesis of fibroblasts from keloid and hypertrophic scar tissue is greater than that from healthy human skin. Tranilast (3-100 μM) did not inhibit prolyl hydroxylase (the rate-limiting enzyme in collagen synthesis) activity. Tranilast (3-300 μM) suppressed the collagen synthesis of fibroblasts from keloid and hypertrophic scar tissue but not healthy skin fibroblasts. Tranilast (30-300 μM) inhibited the release of transforming growth factor (TGF)-β1 from keloid fibroblasts, which enhances the collagen synthesis of keloid fibroblasts. Anti-TGF-β1 antibody (50 μl/ml) inhibited the collagen synthesis, although diphenhydramine (10 μM) and indomethacin (10 μM) did not show any inhibition. These results suggest that tranilast inhibits collagen synthesis of fibroblasts from keloid and hypertrophic scar tissue through suppressing the release of TGF-β1 from the fibroblasts themselves.View full abstractDownload PDF (464K) -
Tadahiro Shikimi, Keisuke Hattori, Shuji Takaori1992 Volume 60 Issue 2 Pages 97-103
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSA human urinary trypsin inhibitor, urinastatin (UT)-like immunoreactive substance with trypsin inhibitory activity, was demonstrated in certain brain regions in rats, especially the cerebral cortex, hippocampus and hypothalamus. Although this UT-like substance in the rat brain displayed an N-terminal amino acid sequence similar to that of glyceraldehyde-3-phosphate dehydrogenase (GAPDH), it did not show any GAPDH activity. These results indicate that the UT-like substance in the rat brain is a protein different from GAPDH and indicates a localized distribution within certain brain regions partly related to learning and memory.View full abstractDownload PDF (1136K) -
Shogo Tokuyama, Masakatsu Takahashi, Hiroshi Kaneto1992 Volume 60 Issue 2 Pages 105-110
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSBased on the data that diazepam, a benzodiazepine (BZP) receptor agonist, antagonized psychological (PSY)-stress induced analgesia (SIA) without prominent action on footshock (FS)- and forced swimming (SW)-SIA and that BZP receptors are coupled with GABA receptors, we examined how the GABAergic system participates in the production of various SIAs. Muscimol, a GABAA receptor agonist, at doses of 0.25 to 1.0 mg/kg, affected each SIA differently, suppressed PSY-SIA at 0.25 mg/kg but tended to potentiate it at 1.0 mg/kg, potentiated SW-SIA dose-dependently and did not affect FS-SIA at the doses employed. Both bicuculline, a GABAA receptor antagonist, 0.5 to 2.0 mg/kg, and picrotoxin, a Cl- channel blocker, 0.25 to 1.0 mg/kg, dose-dependently suppressed PSY-and FS-SIA. Meanwhile, the effects of both drugs on SW-SIA were less than those on PSY- and FS-SIA, namely, bicuculine slightly inhibited it only at 2.0 mg/kg, and picrotoxin did not produce any appreciable effect even at the highest dose. Baclofen, a GABAB receptor agonist, at 5.0 and 10.0 mg/kg had no influence on each SIA. On the contrary, CGP 35348, a GABAB receptor antagonist at 20 to 100 mg/kg caused the dose-dependent blockade of FS-SIA, but affected neither PSY- nor SW-SIA. The production of PSY- and SW-SIA is attributable to the GABAA receptors/Cl channel mediated mechanism alone, while that of FS-SIA involves both GABAA and GABAB receptor mediated systems. Thus, GABAergic systems play an important role in the production of each SIA; however, the participation of the receptor subtypes in the mechanism was different from each other.View full abstractDownload PDF (359K) -
Chikako Shima, Masataka Majima, Makoto Katori1992 Volume 60 Issue 2 Pages 111-119
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSDegradation of bradykinin (BK) in human plasma was investigated by searching for a stable metabolite as a marker of kinin release in vivo. BK, incubated with diluted plasma, was degraded to des-Arg9-BK (des-9-BK), des-Phe8-Arg9-BK (des-8, 9-BK) and Arg-Pro-Pro-Gly-Phe ([1-5]BK). Des-9-13K was degraded to [1-5]BK without an increase in des-8, 9-BK, and des-8, 9-BK was also degraded to [1-5]BK. D, L-2-Mercaptomethyl-3-guanidinoethyl-thiopropanoic acid inhibited the formation of des-9-BK from BK, whereas captopril inhibited the formation of des-8, 9-BK from BK as well as that of [1-5]BK from des-9-BK or des-8, 9-BK. The half lives of BK, des-9-BK, des-8, 9-BK and [1-5]BK under the present experimental conditions were 60 min, 90 min, 14 min and 4.2 hr, respectively. Among the metabolites, [1-5]BK was the most stable one and may be used as a marker for BK production in vivo.View full abstractDownload PDF (493K) -
Mitsutoshi Satoh, Shigeru Ohta, Taku Nagao, Masaaki Hirobe, Hideomi Fu ...1992 Volume 60 Issue 2 Pages 121-125
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSThe amphetamine-related compounds methamphetamine, phenylethylamine and nomifensine increased the K+-evoked release of endogenous noradrenaline from rat spinal cord slices. 4-Phenyl-1, 2, 3, 4-tetrahydroisoquinoline (4PTIQ), which alone did not affect the K+-evoked release of noradrenaline, inhibited the noradrenaline-releasing effects of methamphetamine, phenylethylamine and nomifensine. 4PTIQ revealed a weak noradrenaline-uptake inhibitory effect, and the effect was weaker than those of desipramine and nomifensine. These results showed that 4PTIQ is an antagonist against the amine-releasing effects of amphetamines.View full abstractDownload PDF (335K) -
Katsuhiko Sakitama, Michio Ishikawa1992 Volume 60 Issue 2 Pages 127-131
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSThe effects of morphine-HCl and mephenesin on the flexor reflex mediated by group II afferent fibers were investigated. The flexor reflex was recorded by means of the electromyogram (EMG) evoked in the muscle tibialis anterior by stimulation of the ipsilateral tibial nerve in urethane-α-chloralose anesthetized rats. Afferent volleys corresponding to the phasic EMG component of the flexor reflex with 7.6-msec latency (flexor EMG: fEMG) were also recorded using the double volley technique. The threshold of the afferent volleys mediating the fEMG was approximately twice as high as that of the most excitable afferent volleys, which were considered the spikes of group I afferent fibers, and the conduction velocity of the afferent volleys was 39.9 ± 3.2 m/sec. Morphine-HCl (5 mg/kg, i.v.) did not change the amplitude of the fEMG, but mephenesin (40 and 80 mg/kg, i.v.) depressed it dose-dependently. These results suggest that the fEMG is a flexor reflex mediated by group II afferent fibers, which is not affected by morphine-HCl but depressed by mephenesin.View full abstractDownload PDF (292K) -
Junzo Kamei, Taro Aoki, Hideki Hitosugi, Yuriko Iwamoto, Yutaka Kasuya1992 Volume 60 Issue 2 Pages 133-140
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSThe influence of diabetes on the effects of morphine on the responses of ventrobasal (VB) thalamic neurons to mechanical noxious stimuli were studied in chloral hydrate-anesthetized rats. Animals were rendered diabetic by an injection of streptozotocin (60 mg/kg, i.v.). Morphine (0.3 mg/kg), administered i.v., produced a reduction in the responsiveness of VB thalamic neurons to noxious stimulation in control rats. This effect was reversed by naloxone. In contrast, the inhibitory effects of morphine on the nociceptive responses of VB thalamic neurons were significantly attenuated in diabetic rats, as compared with the controls. However, there were no significant differences in inhibitory potency between diabetic and control rats when morphine (30 nM) was administered intrathecally. It seems likely that these changes in the sensitivity of VB thalamic neurons to morphine are, to some extent, the source of the reduction in the analgesic efficacy of morphine in diabetic rats.View full abstractDownload PDF (415K) -
Yoshikatsu Masuda, Shigeo Murai, Hiroko Saito, Eiichi Abe, Tadanobu It ...1992 Volume 60 Issue 2 Pages 141-144
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESS-Caerulein (CLN, 0.8-80 μg/kg, s.c.) was administered to male rats 10 min or 24 hr before the injection of SKF 38393 (3 mg/kg, i.p.). The increased mouth movement and grooming behavior by SKF 38393 were suppressed dose-dependently by CLN 10 min before the SKF 38393. CLN at the dose of 0.8 μg/kg, given 24 hr before the SKF 38393, suppressed the grooming behavior by SKF 38393. These findings suggest that a low dose of CLN, but not a high dose, had a delayed suppressive effect on the grooming behavior induced by an excess of D1-activity.View full abstractDownload PDF (240K) -
Yumi Sugimoto, Jun Yamada, Ikuko Kimura, Yoshiko Watanabe, Kazuyoshi H ...1992 Volume 60 Issue 2 Pages 145-148
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSThe effects of the serotonin1A (5-HT1A) receptor agonist buspirone on the plasma glucose and pancreatic hormones insulin and glucagon were investigated in rats. Buspirone elicited significant hyperglycemia and hyperglucagonemia, although it did not affect the insulin levels. Adrenodemedullation inhibited both the increase in blood glucose and glucagon levels. These results indicate that buspirone-induced hyperglycemia and hyperglucagonemia are mediated by adrenaline release from the adrenal gland.View full abstractDownload PDF (227K) -
Kenji Asakura, Hanae Ikeda, Munekazu Gemba1992 Volume 60 Issue 2 Pages 149-151
Published: 1992
Released on J-STAGE: June 13, 2006
JOURNAL FREE ACCESSWhen cortical slices prepared from rat kidneys made ischemic were incubated under a 100% oxygen atmosphere, lipid peroxidation increased and the ATP level decreased. Such oxygenation of the slices was accompanied by decreases in gluconeogenesis and the glutathione level, but an anti-oxidant, N, N''-diphenyl-p-phenylenediamine, prevented the increase in lipid peroxidation without affecting decreases in ATP and glutathione levels, and gluconeogenesis. The results suggest that postischemic oxygenation of slices generates free radicals that cause the production of lipid peroxidation not associated with tissue injury.View full abstractDownload PDF (188K)
- |<
- <
- 1
- >
- >|