巻号一覧
31 巻, 1 号
選択された号の論文の22件中1～22を表示しています
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Tetsuhiro HISAYAMA, Issei TAKAYANAGI, Yutaka KASUYA1981 年 31 巻 1 号 p. 1-6
発行日: 1981年
公開日: 2006/11/07
ジャーナル フリーCocaine (3×10-5 M) has been reported to potentiate maximal contraction induced by several stimulants, and this phenomenon might be ascribed to the postsynaptic action. The present study was undertaken to observe the influences of cocaine on Ca-movements, that is, Ca-uptake and Ca-release, in the microsomal fraction of the prostatic half of the rat vas deferens. In this study, it was shown that cocaine potentiated Ca-uptake at the lower concentration (10-6 M) of Ca2+, but had no influence upon Ca-release and also that cocaine significantly increased the rate of Ca-uptake. These results suggest that cocaine promotes binding of Ca ions with the surface sites of smooth muscle membrane concerned with Ca-influx process and thereby potentiates maximal contractions elicited by different stimulants.抄録全体を表示PDF形式でダウンロード (315K) -
Katsuji OGUCHI, Shinichi KOBAYASHI, Tadamasa UESATO, Kazuya KAMIJO1981 年 31 巻 1 号 p. 7-14
発行日: 1981年
公開日: 2006/11/07
ジャーナル フリーKinetical properties of human placental monoamine oxidase (MAO) were investigated in studies on inhibitors and mixed substrates. MAO activity was determined by a radioisotopic assay. Lineweaver-Burk plots were linear at higher and lower concentrations of PEA, whereas at intermediate substrate concentrations, a downward curving plot was obtained. The Km values of the low and high-affinity sites for PEA deamination were estimated. Studies with mixed substrates showed that 5-HT was a competitive inhibitor and tyramine a mixed-type inhibitor of deamination at high concentrations of PEA, whereas both were noncompetitive inhibitors at lower concentrations of PEA. After pre-incubation of human placental mitochondrial preparations with deprenyl, Lineweaver-Burk plots were completely linear, and the Km value was the same as that obtained at low concentrations of PEA in the absence of deprenyl. Tyramine and 5-HT were competitive inhibitors of PEA deamination by deprenyl-treated MAO. From these results it is concluded that there are two kinds of MAO with high- and low-affinity sites for PEA in mitochondria of human placenta, corresponding to type B and A MAO, and that tyramine, 5-HT and PEA share a substrate-binding site on type A MAO, while tyramine and 5-HT bind to a site on type B MAO that is different from the PEA binding site.抄録全体を表示PDF形式でダウンロード (342K) -
Yohko IMAIZUMI, Tatsuyoshi SUGIMOTO, Tsutomu KASAI1981 年 31 巻 1 号 p. 15-21
発行日: 1981年
公開日: 2006/11/07
ジャーナル フリーThe therapeutic effect of diisopropyl 1, 3-dithiol-2-ylidene-malonate (NKK-105) on the fatty liver induced by carbon tetrachloride (CCl4) was studied. The recovery from elevated liver triglyceride levels induced by CCl4 required over 20 days in 35 week-old rats, but 14 days in 6 week-old rats. This indicates that 35 week-old rats are useful for studying the therapeutic effect of NKK-105 on fatty liver. In rats with CCl4-induced fatty liver, NKK-105 lowered the hepatic triglyceride level, accelerated the rate of triglyceride release from the liver, enhanced the incorporation of 14C-leucine into microsomal protein, and increased the RNA content in microsomes. These data suggest that NKK-105 exerts a curative effect on CCl4-induced fatty liver by improving the impaired protein synthesis and by promoting lipoprotein secretion.抄録全体を表示PDF形式でダウンロード (430K) -
Taeko HATA, Tomitaro KITA, Ryozo YONEDA, Seiki TANADA1981 年 31 巻 1 号 p. 23-31
発行日: 1981年
公開日: 2006/11/07
ジャーナル フリーEffects of physical stimulus and psychic stimulus on the galvanic skin response (GSR) in rats were evaluated. A significant change in the GSR was observed after exposing the rat to the noise of hand-clapping, and introducing another rat into the cage. The latter stimulus had a much greater effect than the former. Changes in GSR were measured after various animals were introduced into the test cage. A shift in the GSR in intrusion of guinea pig or rabbit was significantly greater than that in intrusion of Wistar rat, but no difference was observed in intrusion of rat and mouse. Changes in GSR were studied by introducing another animal into the test cage containing a single rat (isolated state) or a pair of rats (grouped state). The change in the GSR in the grouped state was generally smaller than that in the isolated state, but there was no difference in the score between these states when a rabbit was introduced. When the effect of drugs on changing of GSR was investigated, we found that elevation of GSR value, as induced by exogenous stimuli, was inhibited by tranquilizers such as chlorpromazine, carpipramine and diazepam. These tranquilizers in a remarkably small dose had an apparent effect on the psychic, mutual relation in GSR test in rats.抄録全体を表示PDF形式でダウンロード (408K) -
Masahiko HIRAFUJI, Susumu SATOH, Yasumi OGURA1981 年 31 巻 1 号 p. 33-37
発行日: 1981年
公開日: 2006/11/07
ジャーナル フリーWhen prostaglandin E (PGE) contents in kidney medullary tissue were determined, we found that the PGE level was significantly higher in the male rats. The activity of PG synthetase in kidney medullary microsomes to synthesize PGE2 and the effect of treatment with sex hormones on the activity were also investigated. There was no significant difference in PG synthetase activity between male and female intact rats. Subsequently, ovariectomy and orchidectomy were carried out and corn oil (control group), testosterone (2.0 mg/kg) or estradiol (0.2 mg/kg) were given subcutaneously every other day for 2 weeks. Testosterone treatment produced a significant increase in the activity of PG synthetase in males, but not in females, when compared with control values. In contrast, estradiol treatment produced a significant decrease in PG synthetase activity in both sexes. These results suggest that sex hormones may play an important role in the regulation of PG biosynthesis in kidney.抄録全体を表示PDF形式でダウンロード (301K) -
Kyoichi SHIMOMURA, Jo MORI, Fumio HONDA1981 年 31 巻 1 号 p. 39-46
発行日: 1981年
公開日: 2006/11/07
ジャーナル フリーAn intraperitoneal administration of large doses of L-5-hydroxy-tryptophan (L-5HTP) induced dose-dependently a behaviour characterized by backward walking in mice. D-5-hydroxytryptophan (D-5HTP) and L-3, 4-dihydroxyphenylalanine (L-DOPA) in the same doses failed to induce such behaviour. The backward walking induced by L-5HTP was blocked by a decarboxylase inhibitor, DL-α-methyl-DOPA, but was potentiated by a monoamine oxidase inhibitor (MAOI), tranylcypromine or pargyline. An intracerebral injection of L-5-hydroxytryptamine (5-HT) induced a similar backward walking which was potentiated by a MAOI. The backward walking induced by L-5HTP was completely inhibited by 5-HT and dopamine (DA) receptor blockers, but was not inhibited by α- or β-adrenergic blocker, antihistamine or anticholinergic drug. On the other hand, zimelidine and clomipramine, 5-HT uptake inhibitors, markedly potentiated the backward walking, while desipramine had no effect. From the results, it appears that excess amounts of 5-HT formed from L-5HTP produced the backward walking by directly stimulating the central 5-HT receptors, and DA is also involved in the behaviour. This behaviour may serve as a good model to assess the central serotonergic activity of drugs.抄録全体を表示PDF形式でダウンロード (354K) -
Masato SHIBUYA, Naoki KAGEYAMA, Takashi TANIGUCHI, Hiroyoshi HIDAKA, M ...1981 年 31 巻 1 号 p. 47-52
発行日: 1981年
公開日: 2006/11/07
ジャーナル フリーTo further assess the effects of CDP (cytidine diphosphate)-choline on Parkinsonian symptoms, striatal dopamine (DA) was measured fluorometrically in rats after injection of CDP-choline. CDP-choline (300 mg/kg, i.p.) increased the DA content in the striatum (p<0.05) one hour after injection. The behavioral effect of CDP-choline was then tested in rats in which the unilateral nigro-striatal DA neurons had degenerated following an intranigral injection of 6-hydroxydopamine (6-OHDA). CDP-choline alone did not produce behavioral changes in these rats. However, pretreatment with a single dose of CDP-choline (900 mg/kg, i.p.) suppressed both the apomorphine-induced contralateral and the d-amphetamine-induced ipsilateral circling. The same dose of CDP-choline suppressed the number of treadmill revolutions in mice. On the other hand, a 7-day consecutive treatment with 300 mg/kg of CDP-choline enhanced the apomorphine-induced contralateral circling (by 42%, p<0.05). The same treatment with CDP-choline raised the striatal DA content by 29% (p<0.05) on the intact side, but not on the 6-OHDA injected side.These results indicate that CDP-choline has neither a direct nor an indirect DA agonistic effect. The increase in DA content, decrease in locomotion and enhancement of the effect of apomorphine can be explained on the hypothesis that CDP-choline may act as an antagonist on the DA neurons and receptors. The validity of this apparently paradoxical use of CDP-choline with antagonistic effect on DA neurons in the treatment of Parkinson's disease is descussed.抄録全体を表示PDF形式でダウンロード (279K) -
Hiromichi NAKAMUTA, Shinichi FURUKAWA, Masao KOIDA, Haruaki YAJIMA, Ro ...1981 年 31 巻 1 号 p. 53-60
発行日: 1981年
公開日: 2006/11/07
ジャーナル フリーRat brain particulate fraction was found to contain binding sites for 125I-Salmon Calcitonin-I (125I-SCT). Maximum binding occurred in the physiological pH range of 7.25-7.5. The binding reaction proceeded in a temperature-dependent manner. Binding sites were broadly distributed among the various rat brain regions and considerable regional differences existed in the affinity and density as detected by Scatchard analysis. The highest affinity was recorded in the case of the hypothalamus and the lowest in the case of the cerebellum. The KD (nM) and Bmax (pmole/mg protein) estimated for the binding to four regions were as follows: hypothalamus: 1.4 and 0.19, midbrain, hippocampus plus striatum: 1.5 and 0.08, pons plus medulla oblongata: 3.0 and 0.15 and cerebellum: 8.3 and 0.20. Using a particulate fraction of rat brain void of cerebellum and cortices, a binding assay for calcitonins was developed. Binding of 125I-SCT was inhibited by unlabeled salmon, [Asu1, 7]-eel and porcine calcitonins in a dose-dependent manner and the IC50s were 2.0, 8.0 and 30 nM, respectively. The IC50s were comparable to those estimated using a kidney particulate fraction. Human calcitonin, β-endorphin and substance P were weak inhibitors of the binding. Other peptides, drugs and putative neurotransmitters tested (totally 23 substances) failed to inhibit the binding at concentrations of 1.0 μM. The physiological significance of brain binding sites for calcitonin, with the possiblity that the brain may possess endogenous ligands for these sites are discussed.抄録全体を表示PDF形式でダウンロード (441K) -
Tatsuo MIYAUCHI, Kimio KIKUCHI, Susumu SATOH1981 年 31 巻 1 号 p. 61-68
発行日: 1981年
公開日: 2006/11/07
ジャーナル フリーTo study the mechanism of the potentiating effect of lithium chloride (LiCl) on methamphetamine (MA)-induced stereotypy in mice, effects of various drugs on the action of LiCl on the stereotypy and pharmacokinetics of MA in different brain regions and liver were examined. The potentiating effect of LiCl disappeared in mice pretreated with atropine or scopolamine whereas LiCl potentiated the stereotypy in mice pretreated with p-chlorophenylalanine, α-methyl-p-tyrosine, nialamide, physostigmine or butylscopolamine. The concentrations of MA in the striatum, brainstem and liver were increased and the half-life of MA in these tissues was prolonged by LiCl. The effect of LiCl on the kinetics of MA in the brain, but not that in the liver, was blocked by scopolamine. LiCl prolonged the half-life of MA in the brain and liver in mice treated with physostigmine or butylscopolamine. The inhibition of MA elimination from the brain and its blockade by scopolamine seem to explain the potentiating action of LiCl on the stereotypy and the antagonism by scopolamine of the behavioural action of LiCl, respectively.抄録全体を表示PDF形式でダウンロード (396K) -
Hideko TATSUNO-ATODA, Koki SHIGENOBU, Yutaka KASUYA1981 年 31 巻 1 号 p. 69-76
発行日: 1981年
公開日: 2006/11/07
ジャーナル フリーPositive inotropic actions in the normal guinea pig cardiac muscle and the activities required to produce electrical and mechanical responses in the depolarized muscle were examined using epinephrine, dopamine, metanephrine, aminophylline, histamine, serotonin, tyramine, tetraethylammonium (TEA), tetramethylammonium (TMA), and X-537A, a calcium ionophore. In the normal cardiac muscle, histamine produced the greatest positive inotropic action, followed by epinephrine, dopamine and TEA. In the cardiac muscle made inexcitable by the elevated potassium (30 mM), all of the agents tested produced electrical and mechanical responses. Aminophylline was the most potent in the activity to produce the mechanical response in the depolarized muscle; the potencies of histamine, dopamine, X-537A, epinephrine and TEA were much the same. From these results, it was concluded that the positive inotropic effects of the cardiac stimulants are not produced solely through the mechanisms related to the slow channels, but that other mechanisms must be involved in the normal condition where the fast sodium channels are functioning.抄録全体を表示PDF形式でダウンロード (382K) -
Keigo NAKATA, Kazuyoshi KURAHASHI1981 年 31 巻 1 号 p. 77-83
発行日: 1981年
公開日: 2006/11/07
ジャーナル フリーEffects of C-terminal octapeptide of cholecystokinin (C8-CCK) and prostaglandins E1, E2 and F2α on noradrenaline-induced responses and 3H-noradrenaline release in the gallbladder and sphincter of Oddi of guinea pigs were examined. In the sphincter of Oddi, noradrenaline in low concentrations induced a relaxation which was blocked by either phentolamine or propranolol, while noradrenaline in high concentrations induced a contraction which was blocked by phentolamine. These results suggest the existence of excitatory and inhibitory α-receptors and inhibitory β-receptors in the sphincter of Oddi. In the gallbladder, the adrenergic receptors are α-excitatory and β-inhibitory. C8-CCK (10-9 g/ml) potentiated both contractile and relaxing responses to noradrenaline, in the gallbladder. The same concentration of prostaglandins potentiated only contractile response to noradrenaline. In the sphincter of Oddi, noradrenaline-induced responses were not affected by C8-CCK and prostaglandins. Prostaglandins inhibited 3H-efflux evoked by electrical stimulation, while C8-CCK had no effect on the 3H-efflux from both preparations. These results suggest that C8-CCK enhances the contractile and relaxing responses to noradrenaline, and that prostaglandins act in a similar way on the postsynaptic response and, in addition, inhibit presynaptically the release of noradrenaline in the gallbladder. In the sphincter of Oddi, only prostaglandins inhibit the presynaptic event.抄録全体を表示PDF形式でダウンロード (387K) -
Hiroyasu SATOH1981 年 31 巻 1 号 p. 85-93
発行日: 1981年
公開日: 2006/11/07
ジャーナル フリーEffects of local anesthetics (procaine, lidocaine, prilocaine, mepivacaine and bupivacaine) on the sinus node of the nerve-intact dog heart were studied in situ by means of selective perfusion of the sinus node through the sinus node artery. The agents caused a dose-dependent decrease in heart rate and the order of their potency in decreasing the heart rate was as follows, bupivacaine>lidocaine=mepivacaine=prilocaine> procaine. The decrease in heart rate produced by these local anesthetics was not affected by prior administration of atropine. With procaine and prilocaine, the decrease in heart rate was followed by an increase which was inhibited by propranolol given into the sinus node artery or was suppressed in reserpine-pretreated dogs. Tetrodotoxin also prevented the positive chronotropic effect of procaine. From these results the following conclusion can be drawn: the negative chronotropic effects of these agents are induced mainly by a direct inhibitory action on the sinus node, and partly by blockade of sympathetic tone, and the interaction with the postganglionic adrenergic nerves plays an important role in the induction of the positive chronotropic responses to procaine and prilocaine.抄録全体を表示PDF形式でダウンロード (434K) -
Kazuo NAKAMURA, Keiji NAKAMURA1981 年 31 巻 1 号 p. 95-105
発行日: 1981年
公開日: 2006/11/07
ジャーナル フリーAt one week after sino-aortic baroreceptor denervation in the rat, aortic blood pressure and plasma contents of epinephrine and dopamine β-hydroxylase (DBH) activity were elevated during resting and conscious states. Stress-induced elevation of blood pressure and plasma epinephrine were markedly pronounced. These changes disappeared at four weeks after denervation. Sino-aortic deafferentation decreased choline acetyltransferase (ChAc) activity in the nucleus tractus solitarii (NTS) and locus coeruleus (LC) and increased DBH activity, norepinephrine levels, phenylethanolamine N-methyltransferase (PNMT) activity and epinephrine levels in the LC, accompanied with a reduction of DBH activity and norepinephrine contents in the nucleus hypothalamicus posterior. These alterations were confirmed one week after denervation but did not persist for a period of four weeks. At four weeks after denervation, ChAc activity was significantly decreased in the nucleus dorsalis nerve of the vagi but not in the nucleus ambiguus. During the transient hypertensive phase, sino-aortic deafferentation did not alter DBH and PNMT activities in the NTS, A2 cell and A1 cell areas, and both catecholamine levels in the NTS. In conclusion, sino-aortic denervation transiently decreased ChAc activity in the NTS and LC, and enhanced synthesis and accumulation of norepinephrine and epinephrine in the LC accompanied with a decrease in norepinephrine contents and DBH activity in the nucleus hypothalamicus posterior, causally resulting in short-lasting labile hypertension and activation of the adrenal medulla.抄録全体を表示PDF形式でダウンロード (618K) -
Yasusuke MASUDA1981 年 31 巻 1 号 p. 107-116
発行日: 1981年
公開日: 2006/11/07
ジャーナル フリーRat liver microsomes were incubated in the presence of NADPH and CCl4 under various conditions, and losses of glucose 6-phosphatase (G-6-Pase) and cytochrome P-450 were examined in terms of lipid peroxidation and CCl4 metabolism. Loss of G-6-Pase activity correlated well with the enhancement of lipid peroxidation. Loss of cytochrome P-450 was also dependent on the lipid peroxidation, under aerobic conditions. However, the cytochrome was destroyed under anaerobic conditions in which lipid peroxidation and loss of G-6-Pase were greatly suppressed. This anaerobic loss of cytochrome P-450 may be linked with the metabolism of CCl4 by this hemoprotein, as evidenced by the observation that CCl4 metabolism occurred only under anaerobic conditions and was inhibited by carbon monoxide accompanied by the suppression of the loss of cytochrome P-450.抄録全体を表示PDF形式でダウンロード (506K) -
Shingo YANO, Eiichi HOSHINO, Masatoshi HARADA1981 年 31 巻 1 号 p. 117-124
発行日: 1981年
公開日: 2006/11/07
ジャーナル フリーTo make a continuous recording of gastric blood flow (GBF) in rats, application of a cross thermocouple method was investigated together with related pharmacological studies. When secretagogues (tetragastrin, histamine and methacholine) were given intravenously in a dose sufficient to stimulate acid secretion, the increases in GBF observed were much the same as those seen when the aminopyrine clearance technique was used. When epinephrine and norepinephrine were administered via a close intraarterial route in the stomach, there was an initial decrease followed by an increase in the GBF. This biphasic response was antagonized by phentolamine, but not by propranolol, thereby suggesting that those agonists predominantly stimulate α-adrenoceptors. On the contrary, isoprenaline produced an increase in GBF which was attenuated by propranolol. Acetylcholine produced an increase in GBF, which was blocked by atropine. Histamine increased the GBF, and such was inhibited by diphenhydramine, but not by cimetidine, suggesting a stimulation of H-1 receptors by histamine. Serotonin, in a lower dose, and tetragastrin also elicited an increase in GBF. However, with a higher dose of serotonin, there was an increase followed by an apparent decrease in GBF. From these results, it was concluded that the cross thermocouple method is practical for a continuous recording the rat GBF in response to vasoactive drugs.抄録全体を表示PDF形式でダウンロード (404K) -
Akinobu NAGAOKA, Mitsuru KAKIHANA, Hisashi IWATSUKA1981 年 31 巻 1 号 p. 125-127
発行日: 1981年
公開日: 2006/11/07
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Kazuhiko IWATSUKI, Shigetoshi CHIBA1981 年 31 巻 1 号 p. 128-130
発行日: 1981年
公開日: 2006/11/07
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J.L. WILLEMS, M.G. BOGAERT, W. BUYLAERT1981 年 31 巻 1 号 p. 131-133
発行日: 1981年
公開日: 2006/11/07
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Shoichi UEDA, Keiichi IKEGAMI, Ken-ichi YONEMURA, Matao SAKANASHI1981 年 31 巻 1 号 p. 134-136
発行日: 1981年
公開日: 2006/11/07
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Kazumi TAKEYA, Yoshihiro HOTTA, Nobuo HARADA, Gen ITOH, Jinsaku SAKAKI ...1981 年 31 巻 1 号 p. 137-140
発行日: 1981年
公開日: 2006/11/07
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Eiichi HAYASHI, Shizuo YAMADA, Kazumasa SHINOZUKA1981 年 31 巻 1 号 p. 141-143
発行日: 1981年
公開日: 2006/11/07
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Jun HIROI, Jiro SEKI, Minoru OHTSUKA, Shoji KATSUKI, Fumio HONDA1981 年 31 巻 1 号 p. 144-146
発行日: 1981年
公開日: 2006/11/07
ジャーナル フリーPDF形式でダウンロード (145K)
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