巻号一覧
14 巻 (1964)
- 4 号 p. 393-
- 3 号 p. 235-
- 2 号 p. 111-
- 1 号 p. 1-
14 巻, 2 号
選択された号の論文の16件中1～16を表示しています
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今井 祥雄, 荒蒔 義知1964 年 14 巻 2 号 p. 111-117
発行日: 1964/06/01
公開日: 2007/02/09
ジャーナル フリーMany reports have been published on the genesis of hyperlipidemia induced by parenterally administered Triton WR-1339 (Oxyethylated tertiary octylphenol formaldehyde polymer, Winthrop Laboratories, New York), one of the surface-active agents, but the interests were paid especially on hypercholesterolemia (1-10). Frantz et al. (2) and Hirsch et al. (3) described an enhanced rate of hepatic synthesis of cholesterol as the causal factor for the rise of plasma cholesterol level after Triton injection. As an evidence of enhanced cholesterogenesis, further, Hirsch et al. (4) recognized an increase of body total cholesterol could be induced by Triton in mice without any exogenous sources. Meanwhile, Friedman et al. (6) considered the mobilization of cholesterol from body pool was the primary response in this hypercholesterolemia. At present it is a problem to be solved to determine the origin of plasma excess triglyceride after Triton injection, since this change is greater than that of cholesterol itself and the elevation of plasma cholesterol induced by sustained hypertriglyceridemia has been shown by Friedman et al. (5, 6).
The authors in this paper studied on the origin of this plasma excess triglyceride with the use of gaschromatographical analysis of fatty acid composition.抄録全体を表示PDF形式でダウンロード (314K) -
戸田 昇, 藤原 元始, 島本 暉朗1964 年 14 巻 2 号 p. 118-137
発行日: 1964/06/01
公開日: 2007/02/09
ジャーナル フリーIt is generally believed that the cardiac fibers of the right vagus nerve terminate, in large part, near the sinoatrial node and some fibers distribute widely in the atria, and that most of the cardiac fibers of the left vagus supply the atrioventricular node and bundles. On the other hand, there are opposite conclusions regarding the existence of the vagus nerve endings in the ventricles. Electrical stimulation of the vagal fibers to the heart has usually been performed in the open chest animal or in the heart-lung preparation of the dog. Many investigators agree with the inhibitory nature of the vagal innervation on the heart, while there is some evidence for existence of the cardio-accelerator fibers in the vagus nerve (1-4). Middleton et al. (5) have concluded that some vagal fibers make connection with the chromaffin cells or the adrenergic neurons located in or near the heart by demonstrating an adrenaline-like substance in the perfusate of the cat's heart which is responding with the increase in rate and amplitude to vagal stimulation. McEwen (6) has observed an inhibitory effect of vagal stimulation in the rabbit's heart for many hours after the isolation. He, further, has demonstrated that the vagal stimulation restores the normal rhythmicity of contraction in the atria arrested by suspending in the bath for many hours, and that the same vagal stimulation inihibits the regular rhythm restored by the addition of acetylcholine. Using the same type of preparations, Burn and Rand (7) have observed the restarting effect of vagal stimulation on the heart which ceased to beat by cooling.
The marked acceleration of the repolarization phase in the atrial membrane potentials of the dog's and rat's hearts in situ following vagal stimulation has been shown by Hoffman and Suckling (8) and Biersteker et al. (9). Similar observation was made on the turtle's heart in situ by Churney et al. (10). Although the vagal effect on the membrane potentials of the isolated frog's heart was demonstrated by Hutter and Trautwein (11), the vagal effect on the atrial or ventricular membrane potentials of the isolated mammalian heart has not hitherto been presented. During the study of the effect of va, al stimulation on the transmembrane potentials (12), the authors have been confronted with many difficulties which should be previously removed in the isolated atrial preparation with the vagal innervation. Accordingly, the present report concerns with the physiological studies on the effects of vagal stimulation on contraction rate and amplitude in the isolated rabbit's and guinea-pig's atria.抄録全体を表示PDF形式でダウンロード (965K) -
中村 圭二, 増田 義信, 藤本 克郎1964 年 14 巻 2 号 p. 138-149
発行日: 1964/06/01
公開日: 2007/02/09
ジャーナル フリーSince the first finding by Kochakian and Murlin (1), many investigators have coincided in revealing that testosterone produced a positive balance of nitrogen, calcium, potassium and phosphorus in the experimental animals. Hershberger et al. (2) have shown that 19-nortestosterone and its 17-substituted derivative, norethandrolone, exhibit a high myotrophic activity on the levator ani muscle with a considerable high anabolicandrogenic ratio. However, the clinical studies (3) have shown that ethyl derivative of 19-nortestosterone still retains the inherent side effects of anabolic steroids such as androgenic or progestational activities. The present report concerns mainly with anabolic and other hormonal activities of 2α, 17α-dimethyl-19-nortestosterone and its derivatives in the experimental animals.抄録全体を表示PDF形式でダウンロード (542K) -
杉本 治良, 民野 和子, 門川 千代子, 飯田 尚武, 森田 雅夫1964 年 14 巻 2 号 p. 150-160
発行日: 1964/06/01
公開日: 2007/02/09
ジャーナル フリーBy using the intracellular microelectrode technique, Toda (1) reported the effects of adrenaline, noradrenaline and reserpine on transmembrane potentials in pacemaker and non-pacemaker fibers of isolated rabbit atria, and suggested that endogenously liberated adrenaline and noradrenaline play an important physiological role in initiating and maintaining atrial rhythmicity. Further studies on cardiac mechanism were done by Matsuo and Tachi (2) who suggested that the initiating substance in atrial contraction may be adrenaline or noradrenaline in isolated atrial preparation.
On the other hand, Bulbring and Burn (3, 4) concluded that the local formation of acetylcholine initiates auricular contraction. Kottegoda (5) also reported that acetylcholine in a high concentrations had a stimulant action on rabbit atria in the presence of atropine. In rabbit auricles, noradrenaline and acetylcholine were found present in about the same amounts of 1.3 to 1.48 μg/g [Burn (4), Matsuo (6)]. From these observations it may safely be assumed that endogenous acetylcholine is the trigger substance in the release of endogenous adrenaline or noradrenaline which, in turn, initiates atrial movement. Conversely, the depletion of endogenous acetylcholine or noradrenaline in atria may cause the arrest of atrial movement.
Paasonen and Krayer (7) have shown that the administration of reserpine to a dog heart-lung preparation leads to a marked decrease in the noradrenaline content of the heart, but the adrenaline content normally 5 per cent that of noradrenaline shows no clear-cut decrease. This result would indicate that, rather than noradrenaline, endogenous adrenaline may be the more important hormone relative to atrial movement. Kirshner and Goodall (8) have shown that the soluble fraction of adrenal medullary hon ogenates form adrenaline from noradrenaline and L-methionine in the presence of ATP. Pilgeram et al. (9) suggested that the methyl groups of choline may be derived by transmethylation from L-methionine, and that the active formation of phospholipid choline from aminoethanol was obtained only through utilization of the methyl group of L-methionine. It may therefore be assumed that L-methionine is the substance essential both to endogenous adrenaline and acetylchholine, which are the initiators and modulators of atrial rhythmicity. The present experiment was carried out to study the effects of L-methionine on isolated normal, or reserpine or nicotine-treated atria, in order to discover the physiological role of L-methionine in the cardiac mechanism.抄録全体を表示PDF形式でダウンロード (527K) -
佐藤 哲男, 岩本 多喜男1964 年 14 巻 2 号 p. 161-165
発行日: 1964/06/01
公開日: 2007/02/09
ジャーナル フリーSince the presence of serotonin in the brain was first reported by Twarog and Page (1), and Amin, Crawfold and Gaddum (2), serotonin has been approached by many investigators. A number of informations concerning the effects of tranquilizing agents, especially reserpine and its related compounds, on serotonin level in brain have been reported. Brain serotonin is especially associated with reserpine as shown by the evidence that the central actions of reserpine are mediated through serotonin.
In the preceding papers (3, 4), authors reported that the effects of a certain tranquilizing agents on rat brain catecholamine levels in shocked state were investigated, and resulted that some of them, i.e., chlorpromazine, tetrabenazine and azacyclonol showed the effects to inhibit the elevation of catecholamine levels caused by electroshock.
In the present study, the effects of chlorpromazine, tetrabenazine and azacyclonol on rat brain serotonin level in shocked state same conditions as that in the case of catecholamine levels, were investigated.抄録全体を表示PDF形式でダウンロード (210K) -
三須 良実, 高折 修二1964 年 14 巻 2 号 p. 166-180
発行日: 1964年
公開日: 2007/02/09
ジャーナル フリーThe depressive effects of adrenolytics on the transmembrane potentials of isolated atria in the intact and reserpinized rabbits have been described in the previous reports (1, 2). The heart which had ceased to beat by the application of the adrenolytics was easily restarted by the addition of adrenaline or noradrenaline. The recovery of the configuration of atrial non-pacemaker potentials by either amine was usually transient and incomplete, though almost full recovery of the repolarization phase of the potentials was observed. In the reserpinized atria, the action potentials depressed by the adrenolytics also restarted and recovered by the addition of acetylcholine except the rate and repolarization phase. The recovering effects of acetylcholine on the restnig potential and the amplitude and depolarization phase of the action potentials were complete and long-lasting. These results suggested that endogenous acetylcholine maintained the depolarization phase, while endogenous noradrenaline regulated the repolarization phase of the transmembrane potentials.
The stimulating effects of acetylcholine on the spontaneous contraction of the heart have been reported by many investigators (3-8). These effects are likely to derive from endogenous noradrenaline released by acetylcholine since the stimulating effects of acetylcholine are prevented or blocked by the application of dichlorisoproterenol (DCI) or the full reserpinization (3-5 and 9). However, the restarting effects of acetylcholine on the atria of reserpinized rabbits which had been depressed by the adrenolytics were confirmed in the previous report (2). Moreover, it will be shown that the depressed heart by DCI can be restarted by the addition of acetylcholine but not of catecholamines (10). These evidences suggest that acetylcholine stimulates the heart directly but not indirectly through l endogenously released noradrenaline.
On the other hand, the adrenolytics have been reported to affect the effects of acetylcholine in the various structures. Benfey et al. (11) have shown that the adrenolytics block parasympathetic effects of the vagus nerve in the isolated guinea-pig's atria. The blocking effects of di benamine on the pharmacological action of acetylcholine in the aortae and strips of the stomach of rabbits and the isolated auricles of rats have been reported by Furchgott (12). The anti-acetylcholine effects of chlorpromazine have been widely confirmed (13).
The present investigations are attempted to correlate depressive effects of the adrenolytics on the transmembrane potentials of the isolated rabbit's atria with endogenous role of acetylcholine.抄録全体を表示PDF形式でダウンロード (697K) -
松岡 正己1964 年 14 巻 2 号 p. 181-193
発行日: 1964/06/01
公開日: 2007/02/09
ジャーナル フリーThe various pathways for the metabolism of exogenous and endogenous catecholamines have been repeatedly and extensively studied in recent years (1-12). It has been established that circulating catecholamine initially undergoes O-methylation rather than deamination in both man and animals (13, 14). The metabolic pathways of brain catecholamines is a little difference from that of circulating catecholamines. The relative importance of catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) in the inactivation of catecholamines in the brain has been a matter of debate. In the present study it was attempted to investigate the metabolism of noradrenaline which was injected into the cisterna of the rabbit.
Noradrenaline is present in all sympathetic neurons. In recent years electronmicroscopic studies have demonstrated that noradrenaline resides in the electron-dense core of the granulated vesicle in preterminal axons and synaptic endings in the hypothalamus of the rat (15) and of the rabbit (16). The uneven distribution of catecholamines in the brain (17-21) suggests that catecholamines have roles to play in the specialized function of those ragions where its concentration is high. However the precise role for brain catecholamines has not been clearly understood. Reserpine, α-methyl-m-tyrosine, Su 5171, Win 18501-2 and monoamine oxidase inhibitors have been used to try to obtain informations on the function of catecholamines in the brain (22-28). It is well established that the sedative action of reserpine is closely associated with loss of noradrenaline and that of serotonin in the brain (29, 30). However, lack of which amines is responsible for the sedative action of reserpine is open to question. The present experiments were performed on rabbits and mice in order to obtain a better understanding of the central action of reserpine, Win 18501-2, Catron and iproniazid.抄録全体を表示PDF形式でダウンロード (567K) -
松尾 高明, 服部 圭佑, 本庄 俊, 島本 暉朗1964 年 14 巻 2 号 p. 194-200
発行日: 1964/06/01
公開日: 2007/02/09
ジャーナル フリーIn this laboratory, Misu (1) have studied the effects of the adrenolytics on the atrial transmembrane potentials of the isolated rabbit's heart, and have shown that the adrenolytics decrease the rate and amplitude and prolong the total duration of the potentials until the complete disappearance of the potential, and that the abolished potential change is not restarted by the washing-out of the preparation but is restarted by the administration of adrenaline or noradrenaline.
Theses results prompted the current experiments, in which the effects of the intravenous injection of the adrenolytics such as dibenamine, chlorpromazine and yohimbine on the catecholamine content of the various tissues were studied in rabbits in order to elucidate the mode of action of the adrenolytics.抄録全体を表示PDF形式でダウンロード (316K) -
塩屋 明利, 倉石 弘一, 柿本 守夫, 玉真 洋子1964 年 14 巻 2 号 p. 201-214
発行日: 1964/06/01
公開日: 2007/02/09
ジャーナル フリーIn a healthy subject, ammonia produced in the body is excreted by the kidney in the form of urea, the product of the urea cycle (1), or converted into substances useful for the body.
In cases of hepatic disorders, on the other hand, blood ammonia level is known to increase (2-6). It is likely that ammonia in high concentrations interferes with the TCA cycle (7) and thus disturbs the completion of carbohydrate and protein metabolism so seriously as to cause inhibition of ATP synthesis and the subsequent liability or aggravation of fatty degeneration of the liver. It is also possible that the impaired brain metabolism due to elevated blood ammonia is liable to cause disturbance of consciousness or to precipitate coma.
Varieties of treatments lowering the elevated blood level of ammonia have been reported to be effective in relieving the symptoms and improving the pathological conditions of ammonia intoxication. Greenstein et al. (8, 9) and other workers (10-12) dealt with L-arginine ; White and Berenbom (13) and other workers (14-17) studied L-glutamic acid; and Laborit et al. (18-20), Fodor et al. (21), and Tamaki et al. (22) examined Laspartic acid. The findings of these authors support the usefulness of three compounds in reducing the blood level of ammonia, and all three compounds are enjoying clinical use. One may point out the important role of L-ornithine in metabolic process in the body, if he appreciates the critical function of the urea cycle and the TCA cycle. Salvatore and Bocchini (23) obtained an excellent result with concomitant use of Laspartic acid and L-ornithine in protecting the toxic effect of ammonium acetate as compared with the use of L-aspartic acid alone. Salvatore et al. (24, 25) also reported the superiority of the combined medication in chronic intoxication of carbon tetrachloride.
The present paper is concerned with general pharmacology of L-ornithine L-aspartate and effects of the compound upon ammonia and carbon tetrachloride intoxications.抄録全体を表示PDF形式でダウンロード (588K) -
L. LENDLE1964 年 14 巻 2 号 p. 215-224
発行日: 1964/06/01
公開日: 2007/02/09
ジャーナル フリーBläusaure und Schwefelwasserstoff wirken, wenn sic gasförmig inhaliert werden auBerordentlich schnell and beide sind hochtoxische Verbindungen mit einer Wirkun in etwa der gleichen GröBenordnung. Vergiftungen mit beiden Stoffen sind in gewissen Industriezweigen sehr gefurchtet, so z.B. die Blausäure in der Metallurgic and in der Kunststoffproduktion; der Schwefelwasserstoff hat neuerdings auch bei Erdölbohrungen wichtige Vergiftungsmöglichkeiten geboten.
Das Wesen der Blausäurevergiftung gilt als weitgehend geklärt. Man kennt als biochemischen Angriffspunkt das FeIII des Warburgschen Atemfermentes, dessen Blockierung zur inneren Erstickung infolge Aufhebung der Sauerstoffverwertung im Zellstoffwechsel führt. Andere Wirkungsmöglichkeiten treten daneben praktisch ganz zurück. Auch für die Schwefelwasserstoffvergiftung hat man einen gleichen Wirkungsmechanismus vermutet, weil bei in vitro-Versuchen genügende SH2-Konzentrationen auch das Warburgsche Ferment inaktivierten. Neue exakte Untersuchungen am Tier haben aber in Bestätigung der Erfahrungen am vergifteten Menschen these Hypothese nicht bestätigt. Man kennt den biochemischen Wirkungsangriffspunkt von SH2 noch nicht. Auch in der Möglichkeit einer rationellen Vergiftungsbehandlung bestehen wichtige Unterschiede für beide Stoffe.抄録全体を表示PDF形式でダウンロード (438K) -
浅野 牧茂1964 年 14 巻 2 号 p. 225-226
発行日: 1964/06/01
公開日: 2007/02/09
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羽野 寿, 金戸 洋, 角永 武夫1964 年 14 巻 2 号 p. 226-227
発行日: 1964/06/01
公開日: 2007/02/09
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羽野 寿, 金戸 洋, 角永 武夫1964 年 14 巻 2 号 p. 227-229
発行日: 1964/06/01
公開日: 2007/02/09
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熊谷 洋, 酒井 文徳, 福原 武彦, 佐治 美昭, 中西 頴央, 沢辺 隆司, 中川 晄1964 年 14 巻 2 号 p. 229-230
発行日: 1964/06/01
公開日: 2007/02/09
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瀬川 富郎, 小島 康生, 高木 博司1964 年 14 巻 2 号 p. 230-231
発行日: 1964/06/01
公開日: 2007/02/09
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田中 千賀子, 寺岡 章雄1964 年 14 巻 2 号 p. 232-233
発行日: 1964/06/01
公開日: 2007/02/09
ジャーナル フリーPDF形式でダウンロード (105K)
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