巻号一覧
70 巻 (1996)
- 4 号 p. 285-
- 3 号 p. 203-
- 2 号 p. 95-
- 1 号 p. 1-
70 巻, 4 号
選択された号の論文の9件中1～9を表示しています
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Akinori Ueno, Takaki Tokumasu, Hiroaki Naraba, Sachiko Oh-ishi1996 年 70 巻 4 号 p. 285-290
発行日: 1996年
公開日: 2006/04/06
ジャーナル フリーThe injection of lipopolysaccharide (LPS) from E. Coli into the dorsal skin of rats caused a dose-dependent increase in vascular permeability as measured by the extravasation over a 40-min period of intravenously injected dye. This increase caused by LPS was attenuated by pretreatment with the bradykinin (BK) receptor antagonist HOE140, the selective platelet-activating factor (PAF) antagonist TCV309, and by combined treatment with mepyramine and methysergide. Combined treatment with HOE140 and TCV309 resulted in further suppression than that achieved with a single treatment alone. By the simultaneous pretreatment with all antagonists, the response was almost totally abolished. On the other hand, indomethacin also inhibited the response induced by LPS, but not those induced by BK and PAF itself. A small dose of BK or histamine synergistically potentiated the effect of PAF when simultaneously injected. These results suggest that BK, PAF, histamine/serotonin and prostaglandins are involved in the LPS-induced increase in vascular permeability, where PAF, in addition to its direct action, potentiates the response to BK and histamine, and prostaglandins potentiate the actions of other mediators without its direct action.抄録全体を表示PDF形式でダウンロード (417K) -
Koichi Yokota, Noriko Yamamoto, Yuji Obata, Minoru Oda1996 年 70 巻 4 号 p. 291-302
発行日: 1996年
公開日: 2006/04/06
ジャーナル フリーThe effects of the new anti-platelet agent KBT-3022, ethyl 2-[4, 5-bis(4-methoxyphenyl)thiazol-2-yl]pyrrol-1-ylacetate, and its metabolite desethyl KBT-3022 on rabbit neutrophil function were investigated in comparison with the effects of acetylsalicylic acid (ASA), ticlopidine hydrochloride (TP), cilostazol (CIL) and indomethacin (IM). The adhesion and migration of neutrophils induced by formylmethionyl-leucyl-phenylalanine (fMLP) were inhibited by all the compounds tested, their rank order of potency being KBT-3022 = desethyl KBT-3022 > TP = CIL = IM > ASA. KBT-3022, desethyl KBT-3022, CIL and IM all suppressed fMLP-induced increases in the intracellular free Ca2+ concentration ([Ca2+]i) in neutrophils, their potencies correlating with their inhibitory effects on fMLP-induced adhesion and migration. KBT-3022 (1 μM), desethyl KBT-3022 (1-10 μM) and CIL (10 μM) but not IM significantly inhibited both neutrophil migration and the increase in [Ca2+]i induced by leukotriene B4 (LTB4). KBT-3022 (1 μM) and desethyl KBT-3022 (1 μM) suppressed the increase in [Ca2+]i induced by complement C5a. Although KBT-3022 and desethyl KBT-3022 did not influence [3H]LTB4 and [125I]C5a specific binding, [3H]fMLP specific binding was inhibited by desethyl KBT-3022 (IC50: 1.9 μM). Neutrophil adhesion and superoxide anion production stimulated by phorbol 12-myristate 13-acetate were partially inhibited by KBT-3022 (1 μM) and desethyl KBT-3022 (1-10 μM). These results suggest that KBT-3022 and desethyl KBT-3022 have a wider spectrum of action and are more potent inhibitors of neutrophil activation than ASA, TP, CIL and IM.抄録全体を表示PDF形式でダウンロード (858K) -
Hideaki Sada, Takashi Ban, Nicholas Sperelakis1996 年 70 巻 4 号 p. 303-312
発行日: 1996年
公開日: 2006/04/06
ジャーナル フリーTo examine taurine actions on the rate of repolarization of action potentials (AP), L-type Ca2+ (Ica), late outward K+ (IK) and the inward rectifier currents as affected by the external Ca2+ concentrations ([Ca2+]o), whole-cell voltage-clamp and current-clamp experiments were conducted in guinea pig ventricular myocytes. At a high (3.6 mM) [Ca2+]o, 10 mM taurine suppressed both Ica and IK, shortened AP duration and decelerated the rate (−dV/dt) of terminal repolarization of AP. In contrast, at a low (0.9 mM) [Ca2+]o, taurine intensified both Ica and IK, lengthened AP duration and accelerated −dV/dt. However, at either [Ca2+]o, the resting membrane potential was slightly hyperpolarized, and the inward rectifier current examined by the ramp-pulse protocol remained unaffected by taurine. Taurine is suggested to maintain a stable AP duration by altering the inward Ca2+ and IK in the opposite directions, depending on [Ca2+]o. The relevance of the stabilizing action of taurine on the AP duration to its reported antiarrhythmic efficacies is discussed.抄録全体を表示PDF形式でダウンロード (622K) -
Katsuya Fujita, Yasuo Matsumura, Yohko Miyazaki, Masanori Takaoka, Shi ...1996 年 70 巻 4 号 p. 313-319
発行日: 1996年
公開日: 2006/04/06
ジャーナル フリーWe investigated the role of endothelin-1 (ET-1) in the development of hypertension and cardiovascular hypertrophy in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Two weeks after the start of DOCA-salt treatment, the rats were divided into two groups and were given FR139317 [(R)2[(R)-2-[(S)-2-[[ 1-(hexahydro-lH-azepinyl)]-carbonyl]amino-4-methyl-pentanoyl]amino-3-[3-(1-methyl-1H-indolyl)]propionyl] amino-3-(2-pyridyl) propionic acid], a specific ETA-receptor antagonist, or its vehicle for 2 weeks. Uninephrectomized rats without DOCA-salt treatment served as controls. Vehicle-treated DOCA-salt rats developed marked hypertension after 4 weeks. FR139317 significantly suppressed the increase in systolic blood pressure with values averaging 163±8 mmHg (P < 0.05 vs DOCA-salt rats receiving vehicle, 195±9mmHg). Morphological studies in the rats given the vehicle showed vascular medial hypertrophy, with a significant increase in the wall area and wall-to-lumen ratio. A marked decrease in vascular wall hypertrophy was observed in the FR139317-treated DOCA-salt rats. The cardiac hypertrophy in DOCA-salt hypertensive rats was also significantly reduced by FR139317. Therefore, these results suggest that ET-1 plays an important role in the development of DOCA-salt hypertension presumably by stimulating the ETA receptor. In addition, we found that an ETA-receptor antagonist effectively reduced cardiovascular hypertrophy in the rats, so the cardiovascular hypertrophy noted in DOCA-salt hypertensive rats may be related to ET-1.抄録全体を表示PDF形式でダウンロード (657K) -
Juichi Fukuyama, Kiyoshi Ichikawa, Keiji Miyazawa, Shuichiro Hamano, N ...1996 年 70 巻 4 号 p. 321-327
発行日: 1996年
公開日: 2006/04/06
ジャーナル フリーIntimal hyperplasia is a serious problem after percutaneous transluminal coronary angioplasty (PTCA). In this study, we investigated the effects of tranilast on intimal hyperplasia in both in vivo and in vitro experiments. For the in vivo experiments, we used the balloon injury model and the cuff treatment model of rabbits fed regular chow. In the balloon injury model, tranilast decreased intimal area, intima/media ratio, stenosis ratio and vascular DNA content after endothelial injury. Also in the cuff treatment model, tranilast suppressed the intimal hyperplasia. In the in vitro experiments, we assessed the effects of tranilast on platelet-derived growth factor-induced rabbit vascular smooth muscle cell (VSMC) migration and proliferation and on collagen synthesis by VSMCs. Tranilast inhibited VSMC migration, proliferation and collagen synthesis. These results suggest that tranilast has a suppressive effect on intimal hyperplasia after a vascular injury such as PTCA.抄録全体を表示PDF形式でダウンロード (569K) -
Tomoyuki Fujioka, Futoshi Nara, Yoko Shimada, Junichiro Fukushige, Hid ...1996 年 70 巻 4 号 p. 329-335
発行日: 1996年
公開日: 2006/04/06
ジャーナル フリーIn dogs, no significant difference in the reduction of serum cholesterol was observed among three dosing regimens of pravastatin: once in the morning (3 mg/kg), once in the evening (3 mg/kg), and twice-daily (1.5 mg/kg × 2) for 21 days. In rabbits, pravastatin was administered at a dose of 50 mg/kg once-daily given in the evening or 25 mg/kg twice-daily for 14 days; the respective serum and liver cholesterol levels were decreased by 41% and 7% in the once-daily dosing and by 51% and 11% in the twice-daily dosing. The amount of low density lipoprotein (LDL) receptor protein was increased 1.2-1.3-fold (P < 0.05) by both treatments, and no significant difference was noted between these treatment regimens. In addition, there was no significant difference in the extent of up-regulated LDL receptor protein between once-daily dosing in the evening and once-daily dosing in the morning. In the experiments with rabbit hepatocytes, the up-regulated LDL receptor activity induced by preincubation with pravastatin was retained even 24 hr after the removal of pravastatin. These results suggest that the comparable efficacy of pravastatin between once and twice-daily treatment could be explained by retention of up-regulated LDL receptor activity for more than 24 hr in vitro and in vivo.抄録全体を表示PDF形式でダウンロード (514K) -
Takeshi Nabe, Hideki Yamamura, Shigekatsu Kohno1996 年 70 巻 4 号 p. 337-345
発行日: 1996年
公開日: 2006/04/06
ジャーナル フリーEosinophils are thought to be one of the pathophysiologically pivotal cells in atopic-type inflammation. In the present experiments, the in vitro responsiveness to stimuli of eosinophils, which had infiltrated into the airway following intravenous administration of Sephadex G-200 (Sephadex), was mainly studied in non-sensitized and [antigen + Al(OH)3]-sensitized guinea pigs. In sensitized, Sephadex-treated guinea pigs, a large number of eosinophils were found in the bronchoalveolar lavage fluid, whereas a much smaller number of cells were recovered in either non-sensitized or sensitized, Sephadex-untreated animals and a smaller number were recovered in non-sensitized Sephadex-treated animals. The eosinophils from non-sensitized Sephadex-treated guinea pigs released superoxide anion (·O2-) and thromboxane (TX) B2 in response to platelet-activating factor (PAF), leukotriene B4 and Ca ionophore A23187. Either spontaneous or PAF-induced ·O2- generation from eosinophils of sensitized, Sephadex-treated guinea pigs was significantly greater than that from non-sensitized animals, while TXB2 release stimulated by any of the above stimuli was not further enhanced by sensitization. These results indicate that active sensitization can change some eosinophil functions and that the functionally altered cells could play a pathophysiological role in atopic inflammation.抄録全体を表示PDF形式でダウンロード (584K) -
Yoshifumi Hatakeyama, Masaaki Tomoi, Minoru Ohtsuka, Kyoichi Shimomura1996 年 70 巻 4 号 p. 347-350
発行日: 1996年
公開日: 2006/04/06
ジャーナル フリーAdaptive cytoprotection is mediated by diverse mediators and mechanisms. We investigated the implication of capsaicin-sensitive afferent neurons in the adaptive cytoprotection in the rat stomach, taking special notice of nitric oxide, prostaglandins and luminal dilution. Sensory deafferentation abolished the protective effect of capsaicin against 0.6N HCl-induced gastric injury but not the indomethacin-resistant or NG-nitro-L-arginine-resistant adaptive cytoprotection conferred by 0.1 N NaOH. Nor did it attenuate the protection by 0.35N HCl which accompanied luminal dilution. These findings suggest that certain mild irritants do not require sensory neurons to provide nitric oxide- and prostaglandins-mediated adaptive cytoprotection and, furthermore, that capsaicin-sensitive afferent neurons are not crucial, either, so long as there is a contribution of luminal dilution in the adaptive cytoprotection.抄録全体を表示PDF形式でダウンロード (273K) -
Jun Yamazaki, Tetsuro Urushidani, Taku Nagao1996 年 70 巻 4 号 p. 351-354
発行日: 1996年
公開日: 2006/04/06
ジャーナル フリーBa2+ is known to pass through N-methyl-D-aspartate receptor channels and cause an increase in cGMP levels in rat cerebella. In the present study, we compared the activation of rat cerebellar nitric oxide synthase (NOS) by Ba2+ with that produced by Ca2+. Both cations stimulated L-citrulline formation in the presence of calmodulin in identical fractions eluted from an anion exchange column with a salt gradient. EC50 values for Ca2+ and Ba2+ were 200 nM and 50 μM, respectively. The IC50 of NG-monomethyl-L-arginine was the same (200 nM). These indicate a possible action of Ba2+ on NOS through the calmodulin-dependent pathway.抄録全体を表示PDF形式でダウンロード (287K)
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