巻号一覧
60 巻 (1992)
- 4 号 p. 315-
- 3 号 p. 153-
- 2 号 p. 67-
- 1 号 p. 1-
60 巻, 1 号
選択された号の論文の11件中1～11を表示しています
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Shigekatsu Watanabe-Kohno, Hideki Yamamura, Takeshi Nabe, Michiaki Hor ...1992 年 60 巻 1 号 p. 1-8
発行日: 1992年
公開日: 2006/06/13
ジャーナル フリーAntagonistic effects of a newly synthesized compound, (E)-2, 2-diethyl-3''-[2-[2-(4-isopropyl)thiazolyl]ethenyl]succinanilic acid sodium salt (MCI-826) on the contraction of the isolated guinea pig trachea and human bronchus induced by various agonists including peptide leukotrienes (p-LTs), histamine, acetylcholine (ACh), prostaglandin (PG) D2 and others were investigated and compared with the effects of a p-LT antagonist, FPL 55712, in some experiments. MCI-826 potently antagonized LTD4- and LTE4-induced contractions at extremely low concentrations in the isolated guinea pig trachea with pA2 values of 8.3 and 8.9, respectively, on a molar basis. These values indicated that MCI-826 is over 100 times stronger than FPL 55712. Similarly, MCI-826 at 10-8 g/ml (2.4 × 10-8 M) markedly antagonized LTD4-induced contractions of the isolated human bronchus. Although FPL 55712 fairly inhibited the 10-9 g/ml LTC4-induced contraction of the isolated guinea pig trachea, MCI-826 had little effect on the contraction at high concentrations like 3 × 10-6 g/ml (7.1 × 10-6 M). MCI-826 modestly affected the other agonist-induced contractions and the resting tonus of the isolated guinea pig trachea at 10-6 g/ml (2.4 × 10-6 M) or higher concentrations, but FPL 55712 caused fair inhibition of some of those contractions and gradually lowered the resting tonus with time. These results indicate that MCI-826 is a highly potent and selective antagonist of LTD4 and LTE4 and can be a useful tool for biological and pharmacological experiments on p-LTs.抄録全体を表示PDF形式でダウンロード (401K) -
Eriko Aizu, Satoshi Yamamoto, Ryuichi Kato1992 年 60 巻 1 号 p. 9-17
発行日: 1992年
公開日: 2006/06/13
ジャーナル フリーPrimary cultures of mouse epidermal cells (i.e., target cells of skin tumor promotion) stimulated by 12-O-tetradecanoylphorbol-13-acetate (TPA) released prostaglandin E2 within 30 min. Anthralin, a non-TPA type tumor promoter, also stimulated PGE2 release; however, no release was detectable at least up to 4 hr after the addition of anthralin. When the cells were incubated with TPA plus anthralin, both PGE2 and arachidonic acid release were synergistically enhanced. Other non-TPA type tumor promoters, i.e., chrysarobin, 7-bromomethylbenz[α]anthracene, benzoylperoxide, okadaic acid and palytoxin, did not potentiate the TPA-caused PGE2 release. In protein kinase C-down regulated cells, the synergistic stimulation of PGE2 and arachidonic acid release by TPA plus anthralin were not detected. Anthralin plus TPA-did not alter the incorporation of arachidonic acid into cellular phospholipids. Cellular cyclooxygenase activity was increased 2 hr after TPA stimulation. Anthralin-caused increase in cyclooxygenase activity was detected at 6 hr after the addition of anthralin. Cyclooxygenase activity was synergistically increased by treating the cells with TPA plus anthralin. Cycloheximide and actinomycin D inhibited the increase in cyclooxygenase activity caused by anthralin or TPA plus anthralin. These results indicate that anthralin synergistically stimulates TPA-caused PGE2 release by synergistically increasing arachidonic acid release and cellular cyclooxygenase activity.抄録全体を表示PDF形式でダウンロード (607K) -
Masayasu Kimura, Ikuko Kimura, Masashi Muroi, Katsunao Tanaka, Hiroshi ...1992 年 60 巻 1 号 p. 19-24
発行日: 1992年
公開日: 2006/06/13
ジャーナル フリーThe essential moieties in p-phenylene-polymethylene bis-ammonium (PMBA) derivatives, C6H4[X(CH2)nN+R3]2, on the potentiating effects by β-eudesmol, a main component of Atractylodes lancea, of their neuromuscular blockades were investigated in isolated phrenic nerve-diaphragm muscle preparations of normal and alloxan-diabetic mice. PMBA derivatives were separated into the following three groups based on the patterns of the potentiating effects: group I: PMBA-23 (n = 6, R = Me) and PMBA-24 (n = 6, R = Et); group II: PMBA-1 (n = 4, R = Me), PMBA-21 (n = 4, R = Et) and PMBA-2 (X = O, n = 3, R = Me); and group III: PMBA-31 (X = S, n = 3, R = Me), PMBA-3 (X = CO, n = 3, R = Me) and PMBA-4 (X = CHOH, n = 3, R = Me). The pretreatment with 80 μM β-eudesmol for 60 min did not affect group I-induced neuromuscular blocking action, and it potentiated group II and group III-induced ones. The potentiating effect of β-eudesmol on group III was greater in diabetic muscles than in normal ones and that on group II was to the same extent in both muscles. These results suggest that the four-methylene length of the side chains in normal muscles and the hydrophilic moieties adjacent to a phenylene ring in diabetic muscles are related to the potentiating effect by β-eudesmol on PMBA derivatives.抄録全体を表示PDF形式でダウンロード (314K) -
Yoshitaka Uchihashi, Hisashi Kuribara, Sakutaro Tadokoro1992 年 60 巻 1 号 p. 25-31
発行日: 1992年
公開日: 2006/06/13
ジャーナル フリーThe coadministration of ketamine (12.5 mg/kg, but not 3.1 mg/kg, s.c.) with methamphetamine (2 mg/kg, s.c.), cocaine (10 mg/kg, s.c.), scopolamine (0.5 mg/kg, s.c.), caffeine (10 mg/kg, s.c.) and MK-801 (0.1 mg/kg, i.p.) significantly enhanced the ambulation-increasing effects. Furthermore, in the coadministration with morphine (10 mg/kg, s.c.) and GBR-12909 (10 mg/kg, i.p.), not only 12.5 mg/kg but also 3.1 mg/kg of ketamine produced a significant enhancement. On the other hand, the ambulation-increasing effect of ketamine (12.5 mg/kg, s.c.) was significantly suppressed by ceruletide (0.01 mg/kg, i.p.), α-methyl-p-tyrosine (100 and 300 mg/kg, i.p. × 2), nimodipine (1 and 3 mg/kg, i.p.), haloperidol (0.03 and 0.1 mg/kg, s.c.), a low dose of apomorphine (0.1 mg/kg, s.c.), physostigmine (0.1 mg/kg, s.c.) and N6-(L-2-phenylisopropyl)-adenosine (0.1 mg/kg, s.c.). However, imipramine (20 mg/kg, i.p.), 6R-L-erythro-5, 6, 7, 8-tetrahydrobiopterin (100 mg/kg, s.c.), a high dose of apomorphine (0.5 mg/kg), reserpine (0.3 and 1 mg/kg, s.c.), propranolol (0.3 and 1 mg/kg, s.c.), phenoxybenzamine (3 and 10 mg/kg, s.c.) and naloxone (0.3 and 1 mg/kg, s.c.) scarcely interacted with ketamine. These results suggest that ketamine increases the ambulatory activity in mice by facilitating dopamine release from a newly synthesized pool at the presynaptic level, which is affected by a calcium-dependent mechanism.抄録全体を表示PDF形式でダウンロード (462K) -
Kohtaroh Kodama, Shigenobu Shibata, Showa Ueki1992 年 60 巻 1 号 p. 33-38
発行日: 1992年
公開日: 2006/06/13
ジャーナル フリーEffect of minaprine on hypoxia or hypoxia/hypoglycemia (ischemia)-induced impairment of 2-deoxyglucose (2DG) uptake by rat hippocampal slices was evaluated. Since minaprine was found to possess both a stimulating effect on acetylcholine release and a blocking effect on 5-HT2 receptors, the improving effect of minaprine on impaired 2DG uptake was compared to the findings obtained with oxotremorine, ketanserin and pentobarbital. Hippocampal slices were exposed to 20-min ischemia, and then these slices were returned to oxygenated and glucose-containing buffer for 6 hr. Ischemia reduced 30 mM KCl-induced 2DG uptake by the hippocampus. Pretreatment with minaprine, oxotremorine, pentobarbital and ketanserin attenuated the ischemia-induced decline of 2DG uptake. In addition, minaprine, oxotremorine and pentobarbital relatively recovered the increase of 2DG uptake in the hippocampal slices under hypoxia for 45 min. The present results suggest that minaprine exerts a neuroprotective action against ischemia-induced deficit of energy metabolism in vitro.抄録全体を表示PDF形式でダウンロード (442K) -
Sunao Kawano, Nobuhiko Hayashi, Shingo Tsuji, Hideyuki Fusamoto, Taken ...1992 年 60 巻 1 号 p. 39-42
発行日: 1992年
公開日: 2006/06/13
ジャーナル フリーGastric mucosal microcirculatory disturbance in experimental animals is stressed as an important factor in the development of gastric ulceration induced by ethanol. In this study, we used a reflectance spectrophotometry system to investigate the effect of cetraxate on ethanol-induced gastric mucosal hemodynamics in anesthetized dogs. Forty percent ethanol caused a significant increase in the mucosal blood volume and a significant decrease in mucosal hemoglobin oxygenation. The changes in these parameters indicated mucosal congestion and tissue hypoxia. Topical administration of cetraxate (200 mg in 10 ml saline) prevented the increase in mucosal blood volume and decrease in mucosal hemoglobin oxygenation which had been induced by ethanol loading in the stomach. In conclusion, cetraxate showed a protective effect on mucosal microcirculation that resulted in the maintenance of the gastric mucosal integrity against ethanol loading in the gastric mucosa.抄録全体を表示PDF形式でダウンロード (299K) -
Jiro Matsumoto, Koji Ueshima, Tomohisa Ohuchi, Koji Takeuchi, Susumu O ...1992 年 60 巻 1 号 p. 43-49
発行日: 1992年
公開日: 2006/06/13
ジャーナル フリーEffects of chemical ablation of capsaicin-sensitive sensory nerves on functional and mucosal ulcerogenic responses to 2-deoxy-D-glucose (2DG) were investigated in the rat stomach, in comparison with those of indomethacin, a prostaglandin (PG) biosynthesis inhibitor. Intravenous injection of 2DG (200 mg/kg) followed by infusion of this agent (100 mg/kg/hr, i.v.) significantly increased gastric acid secretion and motility, but rarely induced macroscopic damage in the gastric mucosa of normal conscious rats. Chemical ablation of capsaicin-sensitive sensory nerves or pretreatment with in domethacin (5 mg/kg, s.c.) did not significantly affect the acid secretory and motility responses to 2DG, but induced severe hemorrhagic lesions in the stomach within 4 hr. Gastric mucosal blood flow (GMBF) determined by laser Doppler flowmetry under anesthetized conditions did not consistently change during 2DG treatment in any of these three groups, but the rise in GMBF in response to mucosal acidification (0.2 N HCl) was significantly inhibited in the animals pretreated with indomethacin or following chemical deafferentation. We conclude that functional ablation of capsaicin-sensitive sensory neurons, similar to the PG deficiency, increases the gastric mucosal vulnerability during 2DG infusion (acid hypersecretion and hypermotility due to vagal excitation), resulting in hemorrhagic lesions, and that the mechanism may be accounted for at least partly by the impairment of gastric mucosal blood flow response to mucosal acidification.抄録全体を表示PDF形式でダウンロード (470K) -
Emil S. Gabrielian, Sergey E. Akopov, Marina R. Grigorian, Karen S. To ...1992 年 60 巻 1 号 p. 51-54
発行日: 1992年
公開日: 2006/06/13
ジャーナル フリーIschemia-like brain damage was induced in cats by selective injection of 4β-phorbol-12β-myristate 13α-acetate (PMA) into the left carotid artery. PMA-injection provoked significant decreases in platelet and neutrophil counts due to their intravascular aggregation. Platelet and neutrophil aggregates caused brain edema with accumulation of sodium fluorescein in the cerebrospinal fluid and ipsilateral derangement of the cerebral energy state in the parietal cortex. Neurotropin administration decreased the changes in platelet and neutrophil counts and prevented the developments of both brain edema and cerebral energy failure.抄録全体を表示PDF形式でダウンロード (176K) -
Katsuya Yamasaki, Yoshiaki Goto1992 年 60 巻 1 号 p. 55-58
発行日: 1992年
公開日: 2006/06/13
ジャーナル フリーThe effects of DL-β-phenyl-β-alanine (BPBA) on vagal efferent discharges elicited by γ-aminobutyric acid (GABA) and baclofen were investigated in rats. When given alone, BPBA (40 mg/kg, i.v.) caused no significant change in vagal nerve response and did not elicit any convulsions. Pretreatment with BPBA (40 mg/kg, i.v.) resulted in 70% and 80% reductions in the vagal efferent discharges induced by GABA (400 mg/kg, i.v.) and baclofen (4 mg/kg, s.c.), respectively. The present results suggest that BPBA may be a novel GABA antagonist with respect to vagal activation mechanisms in the CNS.抄録全体を表示PDF形式でダウンロード (233K) -
Ikuko Kimura, Takeshi Nagaura, Shinjiro Kobayashi, Masayasu Kimura1992 年 60 巻 1 号 p. 59-62
発行日: 1992年
公開日: 2006/06/13
ジャーナル フリーAnti-proliferative effects of magnoshinin and magnosalin derived from “Shin-i” (Flos magnoliae) were investigated using subcultured endothelial cells (EC) of rat aorta. The inhibitory effects of magnoshinin were 2-fold greater at 10 μg/ml than that of magnosalin on the increase in cell number when EC were stimulated by 5% fetal bovine serum. In the 3H-thymidine incorporation monitored at 3 hr-intervals, magnoshinin (0.1-3 μg/ml) prolonged the starting time of DNA synthesis and reduced the rate of incorporation into EC. Magnosalin (0.3-3 μg/ml) reduced only the incorporation rate. These results suggest that magnoshinin inhibits both the competence phase and progression phase, but magnosalin preferentially inhibits the progression phase in EC proliferation.抄録全体を表示PDF形式でダウンロード (229K) -
Junichi Kurihara, Hiroshi Tomita, Nobuhiko Ochiai, Hitoshi Kato1992 年 60 巻 1 号 p. 63-66
発行日: 1992年
公開日: 2006/06/13
ジャーナル フリーA possible cerebroprotective effect of halothane was investigated in a canine model of 5-min global cerebral ischemia. In pentobarbital-anesthetized dogs, additional inhalation of 0.5 to 1% halothane prior to ischemia prevented the post-ischemic dysfunction of the vagal component of reflex bradycardia. In contrast, pretreatment with thiopental at 10 mg/kg, i.v. failed to prevent it. The influence of ischemia in the absence of anesthetics was similar to that under barbiturate anesthesia. The results suggest that halothane, but not barbiturate, may actively protect the vagal baroreflex system from ischemia.抄録全体を表示PDF形式でダウンロード (237K)
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