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Volume 88 (1986)
- Issue 6 Pages 403-
- Issue 5 Pages 331-
- Issue 4 Pages 255-
- Issue 3 Pages 173-
- Issue 2 Pages 65-
- Issue 1 Pages 1-
Volume 88, Issue 2
Displaying 1-10 of 10 articles from this issue
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Kayoko KUROKI, Tomoko OHSUMI, Yuji MURAKAMI1986 Volume 88 Issue 2 Pages 65-70
Published: 1986
Released on J-STAGE: March 02, 2007
JOURNAL FREE ACCESSGlutaraldehyde (GA) was tested for its cytotoxic effect on L cell tissue culture system in comparison with formaldehyde (FA). In the first study, the replanted cells were grown to monolayers on the flattened bases of the culture tubes, and then exposed to the drug. In the second study, the drug was added to the cell suspension just put in the culture tubes. In either case, the cells were kept in contact with the drug at 37°C for 24, 48 or 72 hr, after which time the monolayers were removed and the viable cells in each of the tubes were counted up. The change in the number of viable cells was examined in the various concentrations of the drugs and time intervals of cell-drug contact. Both GA and FA showed relatively slight toxic effect when each concentration was 1 μg/ml. The cells exposed to 1, 10 μg/ml of GA or 1 μg/ml of FA were able to increase in number, though markedly restrained from their multiplication if compared with the control. GA and FA seriously diminished the viable cells at a concentration of 100 μg/ml and 10 μg/ml, respectively, and they were so toxic that complete cell death was immediately caused even when the concentration of each drug was at 1000 μg/ml. Just replanted cells showed less tolerance to the drug effects than the cells of established monolayers ; suppression of cell growth was noted with the concentration of 0.8 μg/ml and above of either GA or FA, and complete cell death was caused by 58 μg/ml of GA and 7.0 μg/ml of FA. It was clear from these data that both GA and FA were extremely toxic to the tissue culture cells and that the former restrained the cells from growing and from multiplying to a lesser extent than the latter.View full abstractDownload PDF (4205K) -
Hiroyuki KOHNO, Yoshiyuki SEYAMA, Saburo YAMASHITA, Michinori AKASU, H ...1986 Volume 88 Issue 2 Pages 71-76
Published: 1986
Released on J-STAGE: March 02, 2007
JOURNAL FREE ACCESSThe anti-allergic actions of cepharanthine were examined using experimental nasal allergy rats (rhinitis models). In the actively sensitized rhinitis models, leaks of pontamine sky blue (PSB) dye in the perfusate of the nasal cavity were suppressed by cepharanthine treatment. Leaks of PSB dye in the perfusate were also suppressed by ketotifen treatment. β-Glucuronidase activity in the perfusate was lower in the cepharanthine group and in the ketotifen group. In the passively sensitized rhinitis models, leaks of PSB dye in the perfusate were suppressed by cepharanthine treatment. Leaks of PSB dye in the perfusate in the ketotifen group were also suppressed. However, β-glucuronidase activity was not different among the three groups. Cepharanthine (0.025 ?? 25 mg/kg body weight) and ketotifen (0.1 ?? 10 mg/kg body weight) inhibited leaks of PSB into the perfusate in a dosedependent manner. These results suggest that cepharanthine may be clinically effective for treating patients with nasal allergy, and its anti-allergic mechanism may be the same as that of ketotifen.View full abstractDownload PDF (4176K) -
Naohiko ONO, Akihiko SUNAMI, Noriyuki YAMAMOTO, Yasundo YAMASAKI, Hide ...1986 Volume 88 Issue 2 Pages 77-84
Published: 1986
Released on J-STAGE: March 02, 2007
JOURNAL FREE ACCESSAnalgesic and antipyretic effects of proglumetacin maleate (PGM), a new indomethacin (IND) derivative, were investigated in comparison with those of IND on an equimolardose basis. The suppression of phenylquinone-induced writhing in mice by PGM was about 0.8 and 2 times as potent as that by IND when given 1 and 4 hr before the phenylquinone injection, respectively. The analgesic activity of PGM in rat silver nitrate arthritis was about 1.5 times more potent than that of IND. PGM was slightly less active in rat adjuvant arthritic pain than IND. On the other hand, PGM provoked a dose-dependent antipyretic effect on the yeast-induced fever in rats within the dose range without affecting the normal body temperature. Furthermore, PGM showed a significant antipyretic effect on LPS-febrile rabbits. Generally, the antipyretic effect of PGM was moderate as compared with that of IND. These analgesic and antipyretic actions of orally administered PGM may be mainly due to its active metabolite, IND. The above results indicate that PGM may be useful for inflammatory diseases associated with pain and/or fever.View full abstractDownload PDF (5266K) -
Yasuo NAKAO, Haruaki NAKAYA, Morio KANNO1986 Volume 88 Issue 2 Pages 85-94
Published: 1986
Released on J-STAGE: March 02, 2007
JOURNAL FREE ACCESSEffects of nipradilol, a new β-blocker, and its metabolite, denitro-nipradilol, on heart rate and atrioventricular conduction were investigated in anesthetized dogs and were compared with those of propranolol. The β-blocking activity of nipradilol was nearly three times as potent as that of denitro-nipradilol which was almost the same as the β-blocking activity of propranolol. Decrease in heart rate (HR) and prolongation of the atrio-His bundle conduction time (AH) were dose-dependently produced by nipradilol (10, 30 and 100 μg/kg, i.v.), denitro-nipradilol (30, 100 μg/kg, i.v.) and propranolol (30, 100 μg/kg, i.v.). The functional refractory period of the atrioventricular node (AVNFRP) was also prolonged by these drugs in a dose-dependent manner. The changes in HR, AH and AVNFRP were well correlated to their β-blocking activities. However, His bundle-ventricle conduction time (HV) was insignificantly affected by these β-blockers in the doses mentioned above. In the reserpinized and atropinized dogs in which propranolol (100 and 300 μg/kg, i.v.) showed very slight, insignificant influence on HR and AH, nipradilol significantly decreased HR and prolonged AH. AVNFRP was also prolonged significantly by nipradilol. These effects of nipradilol were observed even after the administration of propranolol. Denitro-nipradilol also produced a decrease in HR and prolongations of AH and AVNFRP in reserpinized, atropinized and propranolol-pretreated dogs. These results indicate that nipradilol and its metabolite, denitro-nipradilol, possess a direct depressant action on the sinoatrial node and the atrioventricular node.View full abstractDownload PDF (7866K) -
Hitoshi INABA, Katsuaki KATO, Takashi YANO1986 Volume 88 Issue 2 Pages 95-99
Published: 1986
Released on J-STAGE: March 02, 2007
JOURNAL FREE ACCESSLong term oral administration of trapidil at the doses of 20 and 60 mg/kg/day restored the decrease in motor nerve conduction velocity in genetically diabetic mice (C57BL/KsJ db +/ db +). Trapidil also suppressed the increase in sorbitol content and the decrease in myoinositol content in the sciatic nerve. The elevation of serum total cholesterol level and the decrease in the ratio of serum HDL-cholesterol level to total cholesterol level were suppressed by trapidil. The blood glucose level and the serum triglyceride level were not affected by the drug administration. These results suggest that trapidil may restore the decrease in nerve conduction velocity in diabetic mice through amelioration of the metabolic abnormalities in nerve and microcirculatory disorders.View full abstractDownload PDF (4257K) -
Manabu SHIBATA, Tsuyako OHKUBO, Hiroshi TAKAHASHI, Teruo KUDO, Reizo I ...1986 Volume 88 Issue 2 Pages 101-107
Published: 1986
Released on J-STAGE: March 02, 2007
JOURNAL FREE ACCESSOpiates and opioid peptides were administered in the order of 10-9 ?? 10-6 mol peripherally, and their action on pain sensitivity was investigated by the modified formalin test which has two characteristic pain responses (the first and the second phase) in the mouse hindpaw. Opioid peptides (20 ?? 500 pmol) had dose-dependent analgesia against both first and second phases, and their action ranked dynorphin> [D-Ala2, Met5]-enkephalinamide> [Met5]-enkephalin. EKC and morphine (0.4 ?? 2.5 nmol) inhibited pain response of the first phase, but produced hyperalgesia in the second phase dose-dependently. Lidocaine hydrochloride had peripheral analgesic action, but was about 500 ?? 10000 times weaker than these substances. So, these peripheral analgesic actions have a different mechanism from that of local anesthetic action. N-methyl levallorphan which is thought to be a peripherally selective narcotic antagonist reversed these peripheral analgesic actions at the first and second phases and also prevented the hyperalgesic effects of EKC and morphine at the second phase. Naloxone reversed analgesia at only the first phase. These results suggest that an analgesic mechanism by opioids may exist at the peripheral site as well. Furthermore, it is estimated that a receptor exists which is antagonized by N-methyl levallorphan but not by naloxone and that there is a system of hyperalgesia by EKC and morphine in pain modulation.View full abstractDownload PDF (5015K) -
Yasuo NAGAI, Kiyoshi YOSHIDA, Shigehiko NARUMI, Shigeharu TANAYAMA, Ak ...1986 Volume 88 Issue 2 Pages 109-123
Published: 1986
Released on J-STAGE: March 02, 2007
JOURNAL FREE ACCESSTo investigate the possible action-sites of a cerebral metabolism activator, idebenone (CV-2619), its distribution in the brain and effect on local cerebral glucose utilization (LCGU) were studied both in normal rats (WKY) and in stroke-prone spontaneously hypertensive rats (SHRSP) with cerebrovascular lesions. At 5 min after intravenous administration of [14C] CV-2619 (10 mg/kg), the distribution ratio in the brain was 0.45 ?? 0.56% of the dosage. Autoradiographic study showed that 14C levels were higher in the white matter than in the grey matter. When [14C] CV-2619 was administered orally (100 mg/kg) and intraperitoneally (30 mg/kg), 14C levels in eleven brain regions (15 min after administration) were 0.22 ?? 0.39 μg/g (CV-2619 equivalent) and 1.11 ?? 1.30 μg/g, respectively, in WKY and 0.17 ?? 0.28 μg/g and 1.66 ?? 1.87 μg/g, respectively, in SHRSP. Total 14C levels were not markedly different among the brain regions of the rats. The analysis of unchanged CV-2619 and its metabolites revealed that unchanged CV-2619 in the cerebral cortex, thalamus and cerebellum was relatively higher than that in the other brain regions. Studies on LCGU demonstrated that CV-2619 (30 mg/kg/day, i.p., for 3 days) improved the decrement of LCGU in the temporal cortex, thalamus dorsomedial nucleus, subthalamic nucleus, mamillary body, hippocampus dentate gyrus, caudate-putamen, inferior colliculus and cerebellar nucleus of SHRSP with stroke. Based on these results, the possible action-sites of CV-2619 for its main pharmacological effects were discussed.View full abstractDownload PDF (11336K) -
Arata KUBOTA, Akihiko KUWAHARA, Masano HAKKEI, Keiji NAKAMURA1986 Volume 88 Issue 2 Pages 125-158
Published: 1986
Released on J-STAGE: March 02, 2007
JOURNAL FREE ACCESSDrug dependence tests on a new intravenous anesthesia inducer midazolam were performed in comparison with triazolam in male cynomolgus monkeys utilizing the intravenous route of administration. 1) In the animals trained to self-administer sodium pentobarbital (0.6 ?? 1 mg/kg/inj) under FR1 and FR10 reinforcement schedules, 0.01 midazolam and 0.001 mg/kg/inj triazolam maintained self-administration in more than 4 out of 5 animals under FRI. Doses of 0.03 and 0.001 mg/kg/inj, respectively, were required under FR10. 2) The intradaily progressive ratio test revealed that midazolam maintained self-administration only weakly (equivalently as or more weakly than triazolam did). 3) Midazolam at 0.003 ?? 0.1 and triazolam at 0.0003 ?? 0.01 mg/kg/inj initiated self-administration, respectively, in 3 and 1 out of 4 naive animals, but the numbers of self-administration responses were only slightly higher than the vehicle control level. Pentobarbital at 0.1 ?? 3 mg/kg initiated selfadministration in all of 4 animals with a high level of self-administration. 4) In the single dose suppression test in physically pentobarbital-dependent animals, an ED25 value of midazolam for the suppression of the withdrawal signs was 0.30 mg/kg, i.v., which was almcst equivalent to that for the central nervous system depression (0.27 mg/kg, i.v.). This was in clear contrast to the results of triazolam and pentobarbital, of which the ED25 values for the suppression were lower than those for the central nervous system depression. 5) In naive animals, after the chronic administration of midazolam at 0.9, triazolam at 0.09, pentobarbital at 60 mg/kg/day (the doses inducing intermediate sedation) intravenously for 4 weeks, withdrawal signs were found respectively in 0, 1 and 3 out of 4 animals. After the chronic administration of higher doses of the compounds (1.2, 0.12 and 80 mg/kg/day) for 4 weeks, the withdrawal signs were found respectively in 1 and 2 out of 3 and 3 out of 4 animals. The benzodiazepine antagonist Ro 15-1788 (1 and 3 mg/kg, i.v.) precipitated clear withdrawal signs in none of 3 midazolam animals and 2 out of 3 triazolam animals. From these results, it can be concluded that the drug dependence liability of midazolam is within the range of those of most benzodiazepines.View full abstractDownload PDF (23109K) -
Takeshi KOJA, Masahiro NOMOTO, Takao SHIMIZU, Kanji IZUMI, Takeo FUKUD ...1986 Volume 88 Issue 2 Pages 159-165
Published: 1986
Released on J-STAGE: March 02, 2007
JOURNAL FREE ACCESSTremor induced by TRH and oxotremorine was recorded by a capacitance transducer, and its intensity and frequency were evaluated using power arrays. In mice treated with TRH (20 mg/kg, i.p.), the latency of tremor was 17.1±1.7 min (mean±S.E.) and the duration was 20.4±2.2 min, while the frequency was 13.7±0.3 Hz. In animals with oxotremorine (0.5 mg/kg, i.p.), the latency was 4.3±0.4 min and the duration was 18±2.2 min, while the frequency was 12.7±0.3 Hz. The latter frequency, however, was significantly shifted to a lower frequency as a function of time. In TRH-induced tremor, vertical movements appeared in the same degree as horizontal movements. In oxotremorine-induced tremor, the vertical movements were few, whereas the horizontal movements were observed in a degree similar to those of TRH. The TRH tremor was suppressed by haloperidol and propranolol, but not by atropine. On the contrary, the oxotremorine tremor was inhibited by atropine, but not by haloperidol or propranolol. These results suggest that mechanisms of tremor induced by TRH differ qualitatively from those by oxotremorine; dopaminergic and β-adrenergic receptor mediated functions may be linked to the developments of tremor caused by TRH, while cholinergic systems have a little effect in mice. The apparatus used in this study and power spectral analysis with power arrays may provide a useful method for simultaneous evaluation of the latency, duration, intensity and frequency of tremors.View full abstractDownload PDF (5839K) -
Kohachi KAMATA, Hidemi TODORIKI, Masako KUSUMOTO, Sachiko OH-ISHI, Tak ...1986 Volume 88 Issue 2 Pages 167-172
Published: 1986
Released on J-STAGE: March 02, 2007
JOURNAL FREE ACCESSShort term drug toxicities were investigated using cultures of mouse embryos in the early stage of development. These embryos were collected at the two- or eight-cell stage. They were exposed to bleomycin (Bl) or 6-mercaptopurine (MP) for 24 hr, thereafter, they were grown in BMOC-3 medium without these agents until the blastocyst stage. Total culturing period was 72 hr for the two-cell embryos and 48 hr for the eight-cell embryos. At the end of the culture periods, the number of cells, mitotic index and frequencies of sister chromatid exchange in these embryos after these exposures were unaltered. However, the death rate of embryos was elevated by the exposure to either Bl or MP. These agents are regarded as non-carcinogenic mutagens; therefore, it is suggested that these compounds are lethal to the embryos through an induction of mutation.View full abstractDownload PDF (5344K)
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