巻号一覧
67 巻 (1995)
- 4 号 p. 271-
- 3 号 p. 185-
- 2 号 p. 101-
- 1 号 p. 1-
67 巻, 4 号
選択された号の論文の20件中1～20を表示しています
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Shigeru Furuta, Seiji Toyama, Masahiro Miwa, Takeshi Itabashi, Hiroshi ...1995 年 67 巻 4 号 p. 271-278
発行日: 1995年
公開日: 2006/04/07
ジャーナル フリーPolaprezinc, an insoluble zinc complex of L-carnosine, exhibits anti-ulcer effects by acting directly on mucosal lesions. The disposition of polaprezinc in the stomach was studied to clarify the usefulness of its structure as an insoluble complex. The time courses of 14C-radioactivity in the gastric contents and gastric tissues were parallel to those of 65Zn after oral administration of a mixture of 14-Cpolaprezinc and 65Zn-polaprezinc (14C-, 65Zn-polaprezinc) to rats. The gastric contents of 14C-polaprezinc and 65Zn-polaprezinc were greater than those of 14C-L-carnosine and 65ZnSO4. Mean residence times (MRT) of 14C-polaprezinc and 65Zn-polaprezinc in the stomach were almost the same (ca. 2 hr), and they were double those of 14C-L-carnosine and 65ZnSO4. In gastric tissues, the area under the concentration curves (AUC0-8 hr) of 14C-polaprezinc and 65Zn-polaprezinc were 1.7 times greater than those of 14C-L-carnosine and 65ZnSO4, respectively. After administration of 14C-, 65Zn-polaprezinc to rats with acetic acid-induced ulcers, 14C and 65Zn-radioactivities in the ulcerous sites were very similar and greater than those of 14C-, 65Zn-polaprezinc dissolved in acid. In conclusion, polaprezinc is retained in the stomach longer and adheres to the ulcerous sites more than zinc or L-carnosine. The characteristics of this compound may arise from its insolubility and contribute to its strong pharmacological action.抄録全体を表示PDF形式でダウンロード (536K) -
Hiroshi Mori, Hiroyuki Tanaka, Kenji Kawada, Hiroichi Nagai, Akihide K ...1995 年 67 巻 4 号 p. 279-289
発行日: 1995年
公開日: 2006/04/07
ジャーナル フリーPolaprezinc, an insoluble zinc complex of L-carnosine, exhibits anti-ulcer effects by acting directly on mucosal lesions. The disposition of polaprezinc in the stomach was studied to clarify the usefulness of its structure as an insoluble complex. The time courses of 14C-radioactivity in the gastric contents and gastric tissues were parallel to those of 65Zn after oral administration of a mixture of 14-Cpolaprezinc and 65Zn-polaprezinc (14C-, 65Zn-polaprezinc) to rats. The gastric contents of 14C-polaprezinc and 65Zn-polaprezinc were greater than those of 14C-L-carnosine and 65ZnSO4. Mean residence times (MRT) of 14C-polaprezinc and 65Zn-polaprezinc in the stomach were almost the same (ca. 2 hr), and they were double those of 14C-L-carnosine and 65ZnSO4. In gastric tissues, the area under the concentration curves (AUC0-8 hr) of 14C-polaprezinc and 65Zn-polaprezinc were 1.7 times greater than those of 14C-L-carnosine and 65ZnSO4, respectively. After administration of 14C-, 65Zn-polaprezinc to rats with acetic acid-induced ulcers, 14C and 65Zn-radioactivities in the ulcerous sites were very similar and greater than those of 14C-, 65Zn-polaprezinc dissolved in acid. In conclusion, polaprezinc is retained in the stomach longer and adheres to the ulcerous sites more than zinc or L-carnosine. The characteristics of this compound may arise from its insolubility and contribute to its strong pharmacological action.抄録全体を表示PDF形式でダウンロード (833K) -
Tatsuo Shimizu, Akihiro Aioi, Tomoko Horiguchi, Kiyoshi Kuriyama1995 年 67 巻 4 号 p. 291-295
発行日: 1995年
公開日: 2006/04/07
ジャーナル フリーThe effect of vitamin E on the modulation of keratinocytes was studied in rats. A 1% lauroylsarcosine (LS) ointment caused skin erythema with keratinocyte-damage. A 30% vitamin E ointment markedly alleviated this erythema and protected keratinocytes from cell damage. Vitamin E (100 μg/ml) was also effective on LS (7.5 μg/ml)-induced proliferative reduction of cultured keratinocytes. On the other hand, ointment containing superoxide dismutase (SOD) (99, 000 U/g) decreased the LS-induced erythema, suggesting that superoxide anion (02-) produced from keratinocytes play an important role in the skin irritation. Indeed, LS induced 02- production from cultured keratinocytes. The 02- was significantly reduced by vitamin E and SOD, although vitamin E had no effects on 02- production in a xanthine-xanthine oxidase system, unlike the effect observed with SOD. These results indicate that vitamin E is an inhibitor of keratinocyte-modulation.抄録全体を表示PDF形式でダウンロード (432K) -
Hiroyasu Satoh1995 年 67 巻 4 号 p. 297-304
発行日: 1995年
公開日: 2006/04/07
ジャーナル フリーEffects of phorbol esters, 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and 4-β-phorbol-12, 13-dibutyrate (PDB), that stimulate protein kinase C (PK-C) on the spontaneous action potential and the ionic currents in cultured embryonic chick ventricular cardiomyocytes were examined using whole-cell voltage-clamp and current-clamp modes. Experiments were performed at room temperature (22°C). The firing rate of spontaneous activity was 61.7± 1.6 beats/min (n=12). Phorbol esters (100 nM and 1 μM) caused a negative chronotropic effect, and they inhibited the maximum rate of depolarization and the action potential amplitude. The action potential duration (at 50% repolarization) tended to decrease, and the maximum diastolic potential was unaffected. In whole-cell voltage-clamp experiments, both TPA and PDB inhibited the L-type Ca2+ current and the delayed rectifier K+ current. The fast time constant of the inactivation phase for the Ca2+2+ current was decreased, but the slow component was unaffected. In addition, PDB (100 nM) enhanced the T-type Ca2+ current, accompanied with an increase in its time constant. In contrast, 4-&aipha;-phorbol-12, 13-didecanoate (PDD), an inactive analogue on PK-C, failed to produce significant changes. These results suggest that the PK-C stimulation induced by phorbol esters might affect the ionic currents and modulate the [Ca]i, resulting in regulation of the spontaneous activity of embryonic chick heart cells.抄録全体を表示PDF形式でダウンロード (541K) -
Keiichi Tanaka, Hiroki Kawasaki, Kiyonobu Kurata, Yukihiko Aikawa, Yok ...1995 年 67 巻 4 号 p. 305-314
発行日: 1995年
公開日: 2006/04/07
ジャーナル フリーTo elucidate the mechanism for the selective inhibition of prostaglandin E2 (PGE2) production in inflammatory tissue by T-614 (3-formylamino-7-methylsulfonylamino-6-phenoxy-4H-1-benzopyran-4-one), its effects on both the activity and the induction of cyclooxygenase (COX)-2 were investigated in vitro. T-614 inhibited the activity of purified COX-2 enzyme (IC50: 7.7 μg/ml), but was inactive against both COX-1 activities of microsomal and purified enzymes (IC50: > 300 μg/ml). On the other hand, when the inhibition of PGE2 production by T-614 was examined in the cultured fibroblasts stimulated with bradykinin, T-614 at 1 μg/ml or less inhibited PGE2 release more effectively than that in the above cell-free system. Therefore, we examined which of the COX enzymes was expressed in bradykinin-stimulated fibroblasts by using both the reverse transcriptase-polymerase chain reaction (RT-PCR) and Northern blot analyses. As a result, COX-1 mRNA was constitutively expressed in the cells, whereas COX-2 mRNA was not detected without stimulation with bradykinin, but was expressed within 30 min when stimulated. Furthermore, it was found that the addition of T-614 reduced the COX-2 mRNA levels in 30 min after stimulation. These studies suggest that at least some of inhibitory effects of T-614 on prostanoids production are mediated by the synergy of the inhibition of COX-2 activity and the inhibition of induction, and such an action of T-614 may explain the pharmacological properties of this drug.抄録全体を表示PDF形式でダウンロード (680K) -
Tohru Yasukura, Masafumi Inoue, Takao Irie, Mitsuyoshi Hara, Yoshito M ...1995 年 67 巻 4 号 p. 315-320
発行日: 1995年
公開日: 2006/04/07
ジャーナル フリーAdrenoceptor-mediated Cl- transport in cultured rabbit corneal endothelium was examined using a Cl--sensitive fluorescent dye. The intracellular Cl- concentration ([Cl-]i) in the endothelial cells was estimated to be about 30 mM. Noradrenaline (0.001-0.1 mM) transiently decreased the [Cl-]i in a dose-dependent manner. Such a decrease in [Cl--]i was completely antagonized by pretreatment with the α-adrenoceptor antagonist phentolamine (0.1 mM). The selective α2-adrenoceptor agonist UK 14304-18 (5-bromo-6-[(4H, 5H-imidazol-2-yl)amino]quinoxaline, 0.1 mM) persistently decreased the [Cl-]i, but neither the α1-adrenoceptor agonist phenylephrine (0.1 mM) nor the β-adrenoceptor agonist isoproterenol (0.1 mM) had any effect. The α2-adrenoceptor agonist/antagonist yohimbine (0.1 mM) persistently and more strongly decreased the [Cl-]i than UK 14304-18 did. The yohimbine-induced decrease in the [Cl-]i was not further altered by UK 14304-18 or phenylephrine, but partly reversed by noradrenaline, isoproterenol and an adenylate cyclase activator, forskolin (0.1 mM). The yohimbine-induced decrease in [Cl-]i was inhibited by the carbonic anhydrase inhibitor acetazolamide (1 mM), and Cl--/HC03- exchange inhibitors, 4-acetamido-4'' -isothiocyanostilbene-2, 2'' disulfonic acid and 4, 4'' -diisothiocyanostilbene-2, 2''-disulfonic acid, but not by the H+-ATPase inhibitor N, N'' dicyclohexylcarbodiimide. The forskolin-induced recovery in [Cl-]i was inhibited by the Na+/K+/Cl- cotransport inhibitor bumetanide (0.1 mM), but not by the Cl-channel blocker 5-nitro-2-(3-phenylpropylamino)-benzoic acid. These findings suggest that corneal endothelial cells extrude Cl- upon α2-adrenoceptor stimulation and accumulate Cl- upon β-adrenoceptor stimulation under low [Cl-]i conditions, probably via acceleration of Cl-/HC03- exchange and Na+/K+/ Cl- cotransport, respectively.抄録全体を表示PDF形式でダウンロード (694K) -
Mitsuhiro Narita, Satoru Takahashi, Koji Takeuchi, Susumu Okabe1995 年 67 巻 4 号 p. 321-328
発行日: 1995年
公開日: 2006/04/07
ジャーナル フリーWe examined the effects of chronic treatment with 10 mM sodium taurocholate (TC) on gastric functions, capsaicin-sensitive afferent neurons and the gastric mucosa in male rats. Stomachs were mounted in Lucite chambers, and then the transmucosal potential difference (PD), luminal pH and gastric mucosal blood flow (GMBF) in response to TC or capsaicin was determined. In normal animals, 10 mM TC caused a reduction in PD, and increases in luminal pH and GMBF. Capsaicin (1 mg/ml) produced an apparent increase in GMBF without any change in PD or luminal pH. After 4- or 12-week treatment with TC, the basal PD was significantly reduced, and the luminal pH tended to increase. The increase in GMBF in response to TC or capsaicin was profoundly suppressed in TC-pretreated animals. The calcitonin generelated peptide release in response to capsaicin was significantly reduced after 4 weeks treatment with TC. There were no microscopical changes in the oxyntic mucosa until 4 weeks after TC treatment except for exfoliation of surface cells. However, an increase in inflammatory cell infiltration was observed 12 weeks later. We conclude that chronic treatment with TC causes desensitization of capsaicin-sensitive afferent neurons and reduces GMBF, which may result in the production of gastritis.抄録全体を表示PDF形式でダウンロード (816K) -
Dai Kobayashi, Kazuo Todoki, Satoru Ozono, Eiichiro Okabe1995 年 67 巻 4 号 p. 329-339
発行日: 1995年
公開日: 2006/04/07
ジャーナル フリーThe nature of neurogenic relaxation was investigated in ring preparations of canine lingual artery. In all experiments, the preparations were previously treated with guanethidine (5 × 10-6 M) to block neurogenic constrictor responses. In the presence of norepinephrine (10-5 M) to induce tone, electrical stimulation (10 V, 4 to 16 Hz, for 45 sec) produced relaxation of the rings in an endothelium-independent fashion. The relaxant response in endothelium-denuded rings was not changed by propranolol (10-5 M), and atropine (10-5 M) did not affect the relaxation elicited by electrical stimulation in endothelium-intact rings. NG-monomethyl-L-arginine (10-4 M) or NG-nitro-L-arginine methyl ester (10-4 M), a nitric oxide (NO) synthase inhibitor, had no effect on the electrical stimulation-induced relaxation of endotheliumdenuded rings. Human calcitonin gene-related peptide (CGRP)-(8 - 37) (2×10-8 M), a CGRP1-receptor antagonist, inhibited neurogenic relaxation of endothelium-denuded rings; substance P (10-6 M) failed to mimic the observed effect of electrical stimulation. The demonstrated effect of electrical stimulation was inhibited by glibenclamide (10-5 M), but not tetraethylammonium (2×10-4 M); glibenclamide abolished the relaxation in response to exogenous CGRP or the ATP-sensitive K+ channel opener cromakalim (10-6 M) in endothelium-denuded rings. Moreover, tetrodotoxin (3.13×10-6 M) inhibited the relaxation of endotheliumdenuded rings induced by electrical stimulation. The relaxation was selectively inhibited when endogenous CGRP had been depleted from perivascular nerves by capsaicin (10-6 M). These results suggest that CGRP, but not NO, released from non-adrenergic non-cholinergic nerves by electrical stimulation produces relaxation of canine lingual artery that is mediated by activation of CGRP1 receptors.抄録全体を表示PDF形式でダウンロード (975K) -
Tsutomu Suzuki, Tomohisa Mori, Minoru Tsuji, Miwa Misawa1995 年 67 巻 4 号 p. 341-347
発行日: 1995年
公開日: 2006/04/07
ジャーナル フリーWe recently demonstrated that combining cocaine and morphine could enhance their reinforcing effects which may be mediated by the dopaminergic system. In the present study, the effects of cocaine and morphine on the discriminative stimulus effects of morphine and cocaine, respectively, were examined. Furthermore, dopaminergic mediation in the discriminative stimulus effects of morphine was also examined. Pretreatment with 1.0 or 3.0 mg/kg morphine shifted the dose-response curve for cocaine to the left, and 3.0 mg/kg morphine significantly potentiated the discriminative stimulus effects of cocaine. On the other hand, neither 1.25 nor 2.5 mg/kg cocaine affected the discriminative stimulus effects of morphine. These results suggest that potentiation of the discriminative stimulus effects of cocaine by morphine may reflect the enhancement of reinforcing effects in the combination of cocaine and morphine. Furthermore, neither SCH23390 (D1-receptor antagonist) nor haloperidol (D2-receptor antagonist) affects the discriminative stimulus effects of morphine, while combining these drugs slightly attenuated the effects of morphine. Thus, another neurotransmitter rather than dopamine may play an important role in the discriminative stimulus effects of morphine. Therefore, the discriminative stimulus effects of morphine are apparently not potentiated by cocaine, unlike those of reinforcing effects.抄録全体を表示PDF形式でダウンロード (450K) -
Ken Nagashima, Hideaki Kusaka, Akira Karasawa1995 年 67 巻 4 号 p. 349-357
発行日: 1995年
公開日: 2006/04/07
ジャーナル フリーWe investigated possible renal protective and therapeutic effects of KW-3902(8-(noradamantan-3-yl)-1, 3-dipropylxanthine), a novel and potent adenosine A1-receptor antagonist, on cisplatin-induced acute renal failure (ARF). ARF was induced in rats by a single injection of cisplatin (5 mg/kg, i.v.). Prophylactic treatment with KW-3902 (0.01-1 mg/kg, p.o., twice a day) significantly attenuated the increases of serum creatinine (S-CRE) and urea nitrogen (S-UN) induced by cisplatin. On the other hand, neither furosemide nor trichlormethiazide showed any ameliorating effects against the cisplatin-induced ARF. In the clearance study, the cisplatin-treatment induced marked decreases of glomerular filtration rate (GFR), renal plasma flow (RPF), and reabsorptions of water, sodium and potassium at tubular sites, in comparison with those in untreated normal rats. KW-3902 (0.1 mg/kg, p.o., twice a day) significantly improved these deteriorated glomerular and tubular functions. In the rats with established cisplatin-induced ARF, KW-3902 ameliorated the cisplatin-induced reductions of GFR, RPF, and reabsorptions of water, sodium and potassium at tubular sites. These results suggest that activation of adenosine A1-receptors is involved in the pathogenesis of cisplatin-induced ARF. The adenosine A1-receptor antagonist may be useful for the treatment of cisplatin-induced ARF.抄録全体を表示PDF形式でダウンロード (921K) -
Kohei Sawaki, Kazunori Ouchi, Toshihiro Sato, Mitsuru Kawaguchi1995 年 67 巻 4 号 p. 359-363
発行日: 1995年
公開日: 2006/04/07
ジャーナル フリーTo obtain more insight into the physiological role of gamma-aminobutyric acid (GABA) in rat salivary glands, we measured the concentration of GABA and the activities of its biosynthetic and metabolic enzymes, glutamate decarboxylase (GAD) and GABA transaminase (GABA-T). The GABA concentrations in rat parotid and submandibular glands were 10.0 and 14.3 nmol/g weight, respectively, which were 0.6-0.8% of the levels in the brain (cerebellum and medulla oblongata), whereas glutamic acid (Glu) was abundant in the two glands. These GABA levels in the two glands were significantly decreased by administration of semicarbazide (200 mg/kg, i.p.), a GAD inhibitor, and increased by gabaculine (50 mg/kg, i.p.), a GABA-T inhibitor. The activities of both GAD and GABA-T were also detected in homogenates of the two salivary glands, but they were lower than those in the brain. However, kinetic analysis showed that the values of Michaelis constants for Glu and GABA in both enzyme reactions in these two glands were similar to those in the brain. These results indicate that GABA and its biosynthetic and metabolic enzymes are present in rat salivary glands as well as the brain.抄録全体を表示PDF形式でダウンロード (399K) -
Yoshinori Goto, Kaichi Kida1995 年 67 巻 4 号 p. 365-368
発行日: 1995年
公開日: 2006/04/07
ジャーナル フリーThe effects of chromium compounds on 3-O-methylglucose (3-O-MG) transport were studied in isolated rat adipocytes. Sodium chromate significantly stimulated 3-O-MG uptake into adipocytes in a dose-dependent manner without altering the equilibrium space of 3-O-MG in adipocytes. The stimulatory effect reached the maximum at 300 μM, and the effect was 60-70% of the maximal insulin effect that was obtained with 20 nM insulin. The chromate concentration achieving a half-maximal effect was estimated at 50 μM. The effect of the combination of 1 mM chromate and 20 nM insulin was equipotent to that of 20 nM insulin alone, which showed that these two effects were not additive. The stimulatory effects of 1 mM chromate and 20 nM insulin were entirely abolished in adipocytes deprived of ATP, which indicated that these effects were completely ATP-dependent. Judging from experiments using various chromium compounds, CrO42- was responsible for the insulinomimetic action. These results indicate that the action of CrO42- is exerted through a mechanism analogous to that of insulin action, and that CrO42- is a novel and useful tool for studying issues involved in insulin actions.抄録全体を表示PDF形式でダウンロード (272K) -
Masayoshi Watanabe, Takayuki Ozaki, Yoshihisa Hirata, Osamu Yamamoto, ...1995 年 67 巻 4 号 p. 369-374
発行日: 1995年
公開日: 2006/04/07
ジャーナル フリーLactitol has been reported to decrease the blood ammonia concentration in various experimental hyperammonemia models such as portacaval shunted rats. The mechanism responsible for this lowering of blood ammonia levels was investigated in rats. When lactitol was given orally twice a day for 7 days at doses of 3 and 10 g/kg/day and at half that daily dose on day 8, it significantly decreased the ammonia concentration of the portal blood by 27.3-43.2%, cecal ammonia contents by 49.2-57.6%, and the pH of the cecal contents from 6.52 to 5.92 - 5.54, 4 hr after the final administration. Lactitol also inhibited increases in the portal ammonia concentration induced by the intracecal administration of ammonium acetate (300 mg/kg) 4 hr after the final administration. When lactitol was given orally at bolus doses of 1 and 3 g/kg simultaneously with a charcoal meal, lactitol significantly facilitated small intestinal transit by 12-13%. At a bolus dose of 3 g/kg, given 1 hr before the administration of a charcoal meal into the proximal colon, lactitol significantly facilitated colonic transit by 29.5%. These effects of lactitol were similar to those of lactulose. These findings suggest that lactitol decreases blood ammonia concentration by inhibiting both the production and the absorption of ammonia through reducing intestinal pH and shortening the residence time of intestinal contents in the intestinal tract.抄録全体を表示PDF形式でダウンロード (384K) -
Shigeki Matsubara, Keiko Fushimi, Osamu Kaminuma, Hideo Kikkawa, Norik ...1995 年 67 巻 4 号 p. 375-382
発行日: 1995年
公開日: 2006/04/07
ジャーナル フリーWe examined the relationship between ozone (O3)-induced airway hyperresponsiveness (AHR) and inflammation in guinea pigs. Inhalation of methacholine (MCh) was adopted in the time course study of AHR that was assessed by measuring pulmonary inflation pressure after O3 exposure (3 ppm, for 2 hr) because the degree of AHR detected by inhalation of MCh was greater than that detected by i.v. administration. AHR was detected up to 5 hr after O3 exposure and was not observed at 24 and 48 hr. In the bronchoalveolar lavage (BAL) study, the numbers of neutrophils, eosinophils, lymphocytes and macrophages in BAL fluid (BALF) reached maximum at 24 hr or later. On the other hand, the number of airway epithelial cells in the BALF significantly increased at 2 and 5 hr. In the histological study, disorder and impairment of the airway epithelium in the trachea and lung were observed at 2 and 5 hr. Changes in the airway epithelium were recovered at 48 hr, although an increase in leukocytes was observed in the lung. These results indicate that O3-induced AHR in guinea pigs is most probably associated with impairment of the epithelium rather than with infiltration of inflammatory cells in the airway.抄録全体を表示PDF形式でダウンロード (784K) -
Kazuro Shimakura, Masaki Sanaka, Li-man Wang, Satoru Mineshita, Mizuo ...1995 年 67 巻 4 号 p. 383-389
発行日: 1995年
公開日: 2006/04/07
ジャーナル フリーWe performed this study to demonstrate the experimental procedure for inducing pulmonary edema by angiotensin II (AT II) in rats and to determine the mechanism of hemodynamic pulmonary edema. In the pilot study, 10 μg/ml of AT II was found to be adequate as the edematogenic dose for inducing pulmonary edema. The edematogenic dose of AT II was intravenously given to rats pretreated with 20 mg/kg of an AT II-receptor antagonist, E 4177 (3-[(2''-carboxybiphenyl-4-yl)methyl]-2-cyclopropyl-7-methyl-3H-imidazo[4, 5-b]pyridine), and to rats given 10 mg/kg of an alpha-adrenergic blocker, phentolamine. Similarly, pulmonary edema was induced by 25 μg/ml of adrenaline in rats pretreated with E 4177 (20 mg/kg) and rats with no pretreatment. E 4177 completely suppressed the development of AT II-induced pulmonary edema, whereas phentolamine could not. On the contrary, E 4177 could not suppress the development of adrenaline-induced pulmonary edema. We concluded that AT II-induced pulmonary edema will develop via the specific AT II receptor without the indirect action of adrenaline.抄録全体を表示PDF形式でダウンロード (405K) -
Mitsuhiro Narita, Susumu Okabe1995 年 67 巻 4 号 p. 391-394
発行日: 1995年
公開日: 2006/04/07
ジャーナル フリーWe examined whether or not 4-week treatment with 10 mM sodium taurocholate (TC) weakens the mucosal defensive mechanism in rat stomachs. The ex vivo stomachs of anesthetized animals were perfused with 100 mM HCl. In the control tap water group, mucosal application of 10 mM TC dissolved in 100 mM HCl for 30 min caused a marked increase in gastric mucosal blood flow (GMBF), a reduction in transmucosal potential difference (PD), acid loss and visible mucosal damage. In the TC group, however, acidified TC applied for 30 min caused only a slight increase in GMBF, a reduction in PD, significant acid loss and severe mucosal damage. These results indicate that the mucosal defensive mechanism was extensively weakened after chronic treatment with TC.抄録全体を表示PDF形式でダウンロード (255K) -
Minoru Sugiura, Yukihiro Shoyama, Hiroshi Saito, Kazuho Abe1995 年 67 巻 4 号 p. 395-397
発行日: 1995年
公開日: 2006/04/07
ジャーナル フリーThe effects of ethanol and crocin on the induction of long-term potentiation (LTP) were investigated in the CA1 region of rat hippocampal slices in vitro. Ethanol (50-75 mM) suppressed the LTP induced by strong tetanic stimulation (51 pulses at 100 Hz). Crocin (20 μM) did not affect the baseline synaptic responses, but significantly prevented the LTP-suppressing action of ethanol. This effect of crocin was concentration dependent (10 - 30 μM). Crocin (20 μM) alone did not affect the potentiation induced by weak tetanic stimulation (11 pulses at 100 Hz). These in vitro observations suggest that crocin directly prevents the LTP-suppressing action of ethanol within the hippocampus.抄録全体を表示PDF形式でダウンロード (215K) -
Kaoru Kondo, Hitoshi Hashimoto, Kazuko Sakata, Hiroshi Saga, Jun-ichi ...1995 年 67 巻 4 号 p. 399-401
発行日: 1995年
公開日: 2006/04/07
ジャーナル フリーIn rat hippocampal slices, pituitary adenylate cyclase-activating polypeptide-38 (PACAP-38) stimulated cyclic AMP formation in dose- and time-dependent manners. The PACAP-38 action was dose-dependently attenuated by L-glutamate in the hippocampus; L-glutamate at the concentration of 1 mM attenuated PACAP-38-stimulated cyclic AMP formation by approximately 30%. The inhibitory effect of L-glutamate is also observed in rat cerebellar slices. In contrast, the inhibitory effect of a prostanoid EP3- receptor agonist on PACAP-38-stimulated cyclic AMP formation was brain region-specific; the inhibitory action was observed in the cerebellum but not in the hippocampus.抄録全体を表示PDF形式でダウンロード (222K) -
Makoto Suzuki, Toshio Matsuda, Pranee Somboonthum, Shoichi Asano, Kazu ...1995 年 67 巻 4 号 p. 403-405
発行日: 1995年
公開日: 2006/04/07
ジャーナル フリーEarlier in vivo experiments suggest that serotonin1A (5-HT1A) agonists are new tools for the treatment of experimental cerebral ischemia. The present study examined this idea in an in vitro system. Incubation of rat brain slices under anoxic conditions for 30 min decreased protein synthesis that was assayed in a normoxic medium by measuring the incorporation of [14C]lysine into trichloroacetic acid-insoluble tissue extracts. The 5-HT1A agonists 8-hydroxy-2-(di-n-propylamino) tetralin (10-100 μM) and buspirone (50 μM) attenuated the anoxia-induced decrease in protein synthesis in the slices. Although the degree of the effect is small, it may be relevant to the neuroprotective effect in the in vivo experiments.抄録全体を表示PDF形式でダウンロード (193K) -
Tomohiro Naruse, Ritsuko Ishii, Takeshi Tagawa1995 年 67 巻 4 号 p. 407-410
発行日: 1995年
公開日: 2006/04/07
ジャーナル フリーDevelopment of tolerance to the hypotensive effects of clonidine was investigated in spontaneously hypertensive rats (SHR). Clonidine (125 μg/kg/day) was administered subcutaneously for 5 weeks using an osmotic infusion pump. During the whole infusion period, significant hypotensive and bradycardic effects were observed. Plasma clonidine concentrations were maintained relatively constant at about 2 ng/ml during the infusion period. On termination of treatment with clonidine, both the blood pressure and heart rate rapidly recovered to the control levels. These findings suggest that clonidine does not cause tolerance to its hypotensive effects in SHR with the present administration regimen.抄録全体を表示PDF形式でダウンロード (243K)
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