巻号一覧
62 巻 (1993)
- 4 号 p. 331-
- 3 号 p. 215-
- 2 号 p. 123-
- 1 号 p. 1-
62 巻, 3 号
選択された号の論文の15件中1～15を表示しています
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Giuseppe R. Trimarchi, Francesca A. Arcadi, Roberto De Luca, Claudia I ...1993 年 62 巻 3 号 p. 215-222
発行日: 1993年
公開日: 2006/04/12
ジャーナル フリーWe examined the protective activity of fructose-1, 6-bisphosphate (FBP) on mortality and delayed hippocampal cell death induced by transient cerebral ischemia in the Mongolian gerbil. Forebrain ischemia was produced by bilaterally occluding the common carotid arteries for 15 min using micro-aneurysm clips; then the blood supply to the brain was restored. The number of survivors was counted for 8 days, and the histopathological damage in the CA1 region of the hippocampus was scored according to the semiquantitative scale of Rudolphi and colleagues. When injected 15 min before the ischemic insult, FBP (100 and 333 mg/kg, i.v.) significantly reduced the rate of mortality during the 8-day observation period. Equivalent doses of fructose and fructose monophosphate did not improve survival, and neither did low doses (33 mg/kg) of FBP. FBP also produced a significant degree of protection against the CA1 pyramidal cell loss in comparison with its vehicle (distilled water). Conversely, when we administered the compound, at the same dose, 15 min after the release of the arterial occlusion, we observed neither a significant reduction of mortality nor significant protection against hippocampal CA1 pyramidal cell loss. These results suggest that FBP possesses salutary properties against the damages induced by transient cerebral ischemia, although they are evident only when the compound is administered before the resolution of the ischemic injury.抄録全体を表示PDF形式でダウンロード (595K) -
Mineo Kunihara, Miwako Ohyama, Miyuki Nakano1993 年 62 巻 3 号 p. 223-230
発行日: 1993年
公開日: 2006/04/12
ジャーナル フリーNeurochemical and behavioral investigations were made to assess the role of central dopaminergic systems in mouse locomotor activity and analgesia by spiradoline mesylate. Analgesic activities of the κ-opioid-receptor agonists spiradoline and U-50488H were not altered by haloperidol or L-dopa, whereas morphine analgesia was enhanced by haloperidol but attenuated by L-dopa. Spiradoline decreased spontaneous locomotor activity in mice and inhibited methamphetamine or morphine-induced locomotor activity. In contrast, morphine given alone increased locomotor activity and enhanced methamphetamine-induced locomotor activity. In a neurochemical study, spiradoline decreased the amounts of dopamine metabolites in the striatum, but did not alter them in the brainstem and cerebral cortex. Morphine increased the dopamine metabolite contents in all three brain regions tested. These results suggest that inhibition of the dopaminergic pathway in the brain by spiradoline may be involved in its suppression of locomotor activity, but not in its analgesia; whereas, stimulation of the dopaminergic pathway by morphine seems to function in both behaviors: enhancement of locomotor activity and inhibition of analgesia.抄録全体を表示PDF形式でダウンロード (571K) -
Toshiaki Tamaki, Kouichi Hasui, Yasuharu Aki, Shoji Kimura, Youichi Ab ...1993 年 62 巻 3 号 p. 231-237
発行日: 1993年
公開日: 2006/04/12
ジャーナル フリーWe examined the effects of NG-nitro-L-arginine (L-NNA) on isolated rabbit afferent arterioles to confirm that nitric oxide is released at the resistance vessel level in the kidney. We microdissected the superficial afferent arterioles from the kidneys of New Zealand White rabbits. Each afferent arteriole was cannulated with a micropipette system, and the intraluminal pressure was set at 80 mmHg. By our methods, we found that norepinephrine (NE) decreased the lumen diameter of the afferent arterioles in a dose-dependent manner, and acetylcholine increased the lumen diameter of NE-constricted afferent arterioles. L-NNA (10-4 M) gradually decreased the lumen diameter of afferent arterioles from 21.5±0.9 to 18.6±0.9 μm in 20 min, but NG-nitro-D-arginine (10-4 M) did not affect them (from 21.8±1.3 to 21.8±1.5 μm). L-Arginine (10-4 M) restored the lumen diameter of L-NNA-contracted afferent arterioles to the control levels. These findings indicate that the isolated afferent arteriole has the ability to release or to synthesize and release nitric oxide under basal conditions and that this basal release of nitric oxide plays an important role in the basal tone of the afferent arteriole.抄録全体を表示PDF形式でダウンロード (637K) -
Hideki Okunishi, Keifu Song, Yuko Oka, Toyohide Kobayashi, Tatsuhiko K ...1993 年 62 巻 3 号 p. 239-244
発行日: 1993年
公開日: 2006/04/12
ジャーナル フリーE4177, 3-[(2''-carboxybiphenyl-4-yl)methyl]-2-cyclopropyl-7-methyl-3H-imidazo[4, 5-b]pyridine, was characterized by in vitro autoradiography and by examining functional antagonism upon angiotensin II (Ang II)-induced contraction of isolated vessels. In rat adrenal cortex and liver, E4177 competitively inhibited the specific binding of 125I-[Sar1, Ile8]Ang II, with IC50 being (5.2±1.0)×10-8M for the adrenal cortex and (1.2±0.3)×10-7 M for the liver. These IC50 values were similar to those for losartan, which showed an IC50 of (6.0±0.9)×10-8M for the adrenal cortex and (1.3±0.5)×10-7M for the liver. In contrast, E4177 and losartan had little effect on the binding to rat adrenal medulla where AT2-receptors predominate. These results indicate that E4177 is AT1-specific as is losartan. E4177 and losartan competitively antagonized the Ang II-induced contraction of human and rabbit arterial strips without any agonistic action. The obtained IC50 values indicated that E4177 was twice as potent as losartan in human arteries and three times more so in rabbit aortic strips. Responses to norepinephrine, serotonin, histamine or KCl were not affected by E4177. In addition, E4177 (10-5M) had no effect on angiotensin-converting enzyme activity. These data indicate that E4177 is a potent AT1 Ang II-receptor antagonist that may be clinically useful for the treatment of cardiovascular diseases such as hypertension.抄録全体を表示PDF形式でダウンロード (386K) -
Takashi Nose, Kaito Tsurumi1993 年 62 巻 3 号 p. 245-256
発行日: 1993年
公開日: 2006/04/12
ジャーナル フリーThis study was conducted to quantify the intensity of ultraviolet (UV) erythema in guinea pigs, a method for evaluating anti-inflammatory drugs, and to clarify any correlation of erythema with cutaneous blood flow. Skin color and cutaneous blood flow in non-administered and indomethacin-administered animals were measured by a colorimeter and a laser Doppler flowmeter over time after UV-irradiation treatment. Skin color was indicated by a XYZ colorimetric system and L*a*b* color space. In either colorimetric system, the values of two indices, x and y or a* and b*, increased along with the intensification of erythema. The increase in the chroma (C*) value calculated from a* and b* was UV-dose-dependent. This value was significantly suppressed by indomethacin 0.5-4 hr after irradiation, and it was found to be a clear and sensitive index for evaluating the suppressive effect of drugs. Cutaneous blood flow also increased with UV irradiation. Indomethacin significantly suppressed this increase 2-3 hr after UV irradiation. The changes of cutaneous blood flow correlated with those of C*. These results suggested C* was a suitable parameter to quantify UV erythema, and the change of skin color in UV erythema reflected the change of cutaneous blood flow.抄録全体を表示PDF形式でダウンロード (793K) -
Masaru Kunitomo, Noriko Imaizumi, Emiko Sameshima, Motohatsu Fujiwara1993 年 62 巻 3 号 p. 257-261
発行日: 1993年
公開日: 2006/04/12
ジャーナル フリーWe characterized the pharmacological nature of the tachykinin receptor subtype mediating the contractile response to electrical transmural stimulation (ETS) in the isolated rabbit iris sphincter muscle preparation by using selective NK1-receptor antagonists, spantide and L-668, 169, and a selective NK2-receptor antagonist, L-659, 877. ETS caused a biphasic contraction in this preparation: a rapidly developing cholinergic component followed by a slowly decaying tachykininergic component. The tachykininergic contractile response to ETS was effectively attenuated by spantide and L-668, 169, but only slightly by L-659, 877, indicating that the tachykinin receptors mediating ETS-induced contraction are of the NK1 type. In the same preparation, the contractile activity of substance P (SP) was slightly more potent than that of neurokinin A (NKA). Unlike in other tissues rich in NK1-receptor subtypes, spantide and L-668, 169 antagonized the contractile response to NKA more effectively than that to SP, and the reverse was observed for L-659, 877. These results strongly suggest that the tachykininergic contraction induced by ETS in the rabbit iris sphincter preparation is mediated by NK1-receptors which are activated by endogenously released NKA.抄録全体を表示PDF形式でダウンロード (280K) -
Keiko Maruyama, Noriko Ohkura, Yuko Yagi, Takafumi Nagatomo1993 年 62 巻 3 号 p. 263-267
発行日: 1993年
公開日: 2006/04/12
ジャーナル フリーThe present study was designed to demonstrate the existence in canine aorta of α1-adrenoceptor subtypes, α1High and α1Low, that have different binding affinities for 3H-prazosin and to assess the binding affinity of several drugs for each subtype by a displacement experiment. A radioligand binding assay with 3H-prazosin revealed the presence of two α1-adrenoceptor subtypes in the canine aorta. One of them which has a high affinity for prazosin was designated as α1High (Kd: 12.40 pM, Bmax: 21.88 fmol/mg protein), and the other type was designated as α1Low(Kd: 506.03 pM, Bmax: 88.22 fmol/mg protein). The pKi values of several drugs for each subtype were determined, and all drugs used in the present study, except for benoxathian and chlorethylclonidine, showed significant differences between the pK1 values for α1High and those for α1Low. Although it is difficult to characterize each α1High and α1Low into α1A or α1B by only the displacement potency, one structural characteristic to distinguish between α1High and α1Low could be evaluated.抄録全体を表示PDF形式でダウンロード (342K) -
Taku Taguchi, Keiko Miyake, Kouichi Tanonaka, Manami Okada, Norio Taka ...1993 年 62 巻 3 号 p. 269-278
発行日: 1993年
公開日: 2006/04/12
ジャーナル フリーThe present study was undertaken to explore changes in neurotransmitters and neuromodulators of brain regions impaired by microsphere embolism-induced, sustained ischemia. Nine hundred microspheres (48 μm) were injected into the right internal carotid artery of rats, and the time course of changes in the triphenyltetrazolium chloride (TTC)-stained areas of their brain slices and acetylcholine and amino acid contents in the cerebral cortex, striatum and hippocampus of both hemispheres were determined. The TTC-unstained area, a measure of infarction, was developed in the right hemisphere by the 3rd day after the embolism, which was similar to that on the 28th day. A marked decline in acetylcholine content of these three regions of the right hemisphere was detected throughout the experiment (28 days). The glutamate, aspartate, GABA, and taurine levels were markedly decreased following microsphere-embolism. Most of these decreases were significantly attenuated during the first 5 days following the embolism, and they then partially recovered with time after the operation. Minor metabolic changes were observed in the left hemisphere. The results suggest that microsphere-embolism induces cerebral infarction and/or sustained damage to acetylcholine and neurotransmitter amino acid synthesis and/or catabolism of the brain regions. This model may provide information concerning the pathophysiological alterations in long-term cerebral ischemia and infarction.抄録全体を表示PDF形式でダウンロード (699K) -
Yoshinobu Takata, Fumiki Shimada, Hitoshi Kato1993 年 62 巻 3 号 p. 279-287
発行日: 1993年
公開日: 2006/04/12
ジャーナル フリーBy using rat brain cortical slices preloaded with [3H]norepinephrine, we examined whether ATP-sensitive K+ channels are involved in altered adrenergic neurotransmission during hypoxia. The tritium overflow evoked by transmural nerve stimulation (TNS) was significantly inhibited at 5 min of hypoxia and reached the maximum inhibition at 20 min. The inhibition of the TNS-evoked tritium overflow under a 20-min hypoxia was reversed by subsequent reoxygenation and was concentration-dependently antagonized by glibenclamide (0.1 and 1 μM). 86Rb+ efflux was increased after introduction of hypoxia and reached the peak value at about 20 min, which was concentration-dependently antagonized by glibenclamide (0.1-10 μM). Hypoxia decreased cortical ATP content. Linear correlations were mutually observed among the changes by hypoxia in the TNS-evoked tritium overflow, tissue ATP content and 86Rb+ efflux. The spontaneous tritium outflow was inhibited only after hypoxic periods of more than 16 min, the inhibition being reversed by reoxygenation and antagonized by 1 μM glibenclamide. These results suggest that the inhibition of rat central adrenergic neurotransmission during hypoxia may be associated with an activation of ATP-sensitive K+ channels.抄録全体を表示PDF形式でダウンロード (719K) -
Tomie Kawada, Hsiao-Tung Sun, Mikio Nakazawa, Shoichi Imai1993 年 62 巻 3 号 p. 289-296
発行日: 1993年
公開日: 2006/04/12
ジャーナル フリーThe effects of lacidipine (LC), a new dihydropyridine calcium antagonist, were studied in comparison with those of nifedipine (NF) in isolated arteries of the dog (DG-AR) and isolated aorta (GP-AO), left and right atria (GP-LA, GP-RA) and ventricular papillary muscles (GP-PM) of the guinea pig. In DG-AR precontracted with high K+, LC and NF produced a concentration-dependent relaxation. The relaxant effect of LC was most potent in the basilar artery. The calcium antagonistic effects of LC was 8.7 and 2.1 times more potent than those of NF, in GP-AO and GP-LA, respectively. Thus, LC was about 4 times more selective towards vascular smooth muscles than NF. The negative chronotropic effects in GP-RA and the negative inotropic effect in GP-PM of NF were more pronounced than those of LC. NF was more potent in inhibiting the action potential of GP-PM than LC both in normal polarized and depolarized conditions. The effects of LC were long-lasting. These results suggest that LC is a potent, highly vascular-selective calcium antagonist with little cardiodepressant effects and as such may be suitable for the treatment of hypertension.抄録全体を表示PDF形式でダウンロード (586K) -
Hidenori Yazawa, Kazuo Honda1993 年 62 巻 3 号 p. 297-304
発行日: 1993年
公開日: 2006/04/12
ジャーナル フリーα1-Adrenoceptors in the rat prostate were characterized by a binding assay using the newly synthesized radioligand [3H]-YM617 (5-[2-[[2[ethoxyring(n)-3H](o-ethoxyphenoxy)ethyl]amino] propyl]-2-methoxybenzenesulfonamide HCl) and an in vitro assay. Specific [3H]-YM617 binding in the rat prostate was saturable and of high affinity (KD = 61.5±5.9 pM) with 23.2±6.9 fmol/mg of protein as the maximal number of binding sites (Bmax). α-Adrenoceptor agonists and antagonists inhibited the binding of the radioligand with the following order of effectiveness: YM617 > prazosin = bunazosin > WB4101 >5-methyl-urapidil = phenoxybenzamine > phentolamine > S(+)-isomer of YM617 > yohimbine > norepinephrine > phenylephrine>methoxamine. α1-Adrenoceptors in the rat prostate preferred the R(-)-isomer of YM617 to the S(+)-isomer. Preincubation with chlorethylclonidine (CEC; 10-5M, 10 min) just slightly changed the Bmax value for [3H]-YM617 without changing the KD value in the prostate; however, CEC reduced the Bmax in the aorta. In the isolated tissue, pretreatment with CEC (10-5M, 10 and 30 min) time-dependently shifted to the right the dose-response curve for phenylephrine and decreased the maximal contraction of aortas induced by phenylephrine, but did not shift or decrease those of prostates. The present results indicate that the α1-adrenoceptors in the rat prostate are mainly CEC-insensitive (α1A), whereas those in the aorta are CEC-sensitive (α1B).抄録全体を表示PDF形式でダウンロード (534K) -
Hideto Sasaki, Eiichiro Okabe1993 年 62 巻 3 号 p. 305-314
発行日: 1993年
公開日: 2006/04/12
ジャーナル フリーTo understand the direct involvement of hydroxyl radical (·OH) in the modification of functional reactivity in isolated rabbit lingual artery ring preparations, this study was undertaken to examine the effect of ·OH generated from dihydroxy fumarate (DHF) plus Fe3+-ADP or from H2O2 plus FeSO4· When vasodilators (acetylcholine and nitroglycerin) were given after the ·OH-generating system was removed from the organ chamber, the earlier ·OH exposure produced an attenuation of the ring relaxation induced by acetylcholine but not that by nitroglycerin. Moreover, the earlier ·OH exposure attenuated caffeine-induced contraction and depressed the phasic response, but potently enhanced the tonic response of norepinephrine-induced contraction. Both the enhanced tonic response of KCl-induced contraction produced by earlier ·OH exposure and norepinephrine-induced contraction was inhibited by nisoldipine. These results are consistent with the view that ·OH radicals can potentiate the voltage-dependent influx of Ca. It is also postulated that ·OH may damage sarcoplasmic reticulum (SR) function in the smooth muscle cells, thus reducing Ca release from the SR (this may be reflected by the attenuation of the phasic response), and may selectively attenuate endothelium-dependent relaxation as opposed to endothelium-independent relaxation.抄録全体を表示PDF形式でダウンロード (691K) -
Toyokazu Isono, Natsuki Sato, Yasushi Koibuchi, Shigeru Sakai, Takao Y ...1993 年 62 巻 3 号 p. 315-324
発行日: 1993年
公開日: 2006/04/12
ジャーナル フリーThe anti-ischemic heart effect of (±)-(E)-4-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexenamide (FK409), a novel nitric oxide donor, was studied in dog and rat preparations in vivo and in vitro. In anesthetized dogs with partially occluded coronary artery that were subjected to atrial pacing at a constant blood pressure, FK409 (1-100 μg/kg, i.v.) suppressed the ST-segment elevation on epicardial electrocardiograms. Glyceryl trinitrate (GTN; 10, 32 μg/kg) or dipyridamole (1000 μg/kg) failed to suppress the ST-segment elevation, although continuous i.v. infusion of GTN (32, 100 μg/kg/min) was effective. FK409 also suppressed the ST-segment elevation induced by methacholine in anesthetized rats by both i.v. (10, 100 μg/kg) and intraduodenal (i.d., 100, 1000 μg/kg) injections, while GTN (100 μg/kg, i.v.; 1000 μg/kg, i.d.) was effective only by the i.v. route. FK409 (0.32 μg/kg/min, i.v.) and GTN (10 μg/kg/min) increased the blood flows of the endomyocardium (ENDO) and the epicardium (EPI) and the flow ratio of ENDO/EPI in the ischemic zone in anesthetized dogs with occluded coronary artery. Furthermore, in isolated dog vascular preparations, FK409 (4.6×10-10-4.6×10-7M) had a greater vasorelaxing effect on the large coronary artery [2.0-2.5-mm outer diameter (od)] than on the small coronary artery (0.3-0.5-mm od) or the saphenous artery. The results suggest that FK409 protects against acute experimental myocardial ischemia through relaxation of the large conductive coronary artery, and may be a useful oral drug for the treatment of angina pectoris.抄録全体を表示PDF形式でダウンロード (684K) -
Kunihiko Endo, Katsuya Morita, Yoshiko Uchiyama, Kazuaki Takada, Akira ...1993 年 62 巻 3 号 p. 325-328
発行日: 1993年
公開日: 2006/04/12
ジャーナル フリーInfluences of drug-induced manipulations of central serotonergic function on lidocaine- and pentylenetetrazol (PTZ)-induced convulsions were examined in mice. Agents that suppressed serotonergic transmission increased, whereas drugs that facilitated serotonin (5-HT) function decreased the incidence of lidocaine-induced convulsions. These treatments had similar influences on the incidence of PTZ-induced convulsions. Lidocaine (10-5-10-3M) reduced the stimulation evoked [3H]5-HT release from cortical slices, followed with an increased spontaneous [3H] overflow at higher concentrations. These results may suggest that brain 5-HT neurons are causally involved as inhibitory neurons in lidocaine-induced convulsions as in the case of PTZ-induced convulsions.抄録全体を表示PDF形式でダウンロード (297K) -
Mitsuhiro Nagata, Yoshitsugu Osumi1993 年 62 巻 3 号 p. 329-330
発行日: 1993年
公開日: 2006/04/12
ジャーナル フリーWe investigated the subtype of α-adrenoceptors participating in central noradrenergic inhibition of gastric motility in urethane-anesthetized rats. Noradrenaline at 10 nmole administered intracisternally (i.c.) significantly decreased gastric motility. Yohimbine at 10 nmole, i.c., but not the same dose of prazosin, abolished this noradrenaline-induced decrease in gastric motility. Clonidine at 10 nmole, i.c., but not phenylephrine at 20 nmole, significantly decreased gastric motility. These results suggest that α2-adrenoceptor-mediated mechanisms in the brain stem are involved in noradrenergic inhibitory regulation of gastric motility.抄録全体を表示PDF形式でダウンロード (129K)
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