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Volume 5, Issue 1
Displaying 1-8 of 8 articles from this issue
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AKIRA DOMAYE1955 Volume 5 Issue 1 Pages 1-10
Published: 1955
Released on J-STAGE: February 16, 2007
JOURNAL FREE ACCESSThere have been many studies on the respiratory action of nicotine. As early as in 1919, M. Ozolio de Almeida (1) pointed out that intravenous administration of nicotine gave rise to a sequence of following respiratory reactions: a primary arrest, a short period of acceleration, and then a long arrest of respiration, the last being descrived as “l'apnée nicotinique.” Later, the brilliant works of C. Ileymans et al. (2) proved that the respiratory stimulation of nicotine was accounted for by the chemoreceptor reflex from the carotid and aortic bodies in origin, but the depressant action, especially the mechanism of the two apnoeas caused by nicotine, has not yet been clearly elucidated in spite of their characteristic features. The author analyzed the mechanism of these actions of nicotine on respiration as a part of the “Studies on the Autonomic Reflexes” being conducted in our laboratory, and obtained some newer results including the findings concerning blockade of the nicotine action by hexamethonium.View full abstractDownload PDF (705K) -
SHOICHI IIDA, SHUNJI TAMURA1955 Volume 5 Issue 1 Pages 11-16
Published: 1955
Released on J-STAGE: February 16, 2007
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TATSUO KASAI1955 Volume 5 Issue 1 Pages 17-26
Published: 1955
Released on J-STAGE: February 16, 2007
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TOSHITAKE MUTO1955 Volume 5 Issue 1 Pages 27-41
Published: 1955
Released on J-STAGE: February 16, 2007
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KIYOSHI TANAKA, MUTSUHIRO YASUKATA, ZOROKU OTSUBO1955 Volume 5 Issue 1 Pages 42-47
Published: 1955
Released on J-STAGE: February 16, 2007
JOURNAL FREE ACCESSEarlier concepts on the central action of procaine appear to have been limited to such untoward effects as restlessness, tremor and convulsion. Clinical experiences during the past decade, however, have revealed the usefulness of procaine as an analgesic when administered intravenously in a nontoxic dose. Bigelow and Harrison (1) evidenced this effect experimentally by the measurement of cutaneous pain threshold in human subjects. As Goodman (8) and Keats et al. (15) pointed out, such an action cannot be attributed, to the local action on sensory nerves, since the concentration of procaine in the peripheral tissue should be far below the minimal concentration necessary for nerve block. This naturally leads to the concept that the central nervous system should be responsible for the procaine analgesia.
Despite the wide clinical uses of intravenous procaine (9), there has been no investigator who found pharmacologically any distinct action of procaine on the central nervous system, except excitatory effects, in experimental animals. The present investigation is an attempt to discover depressant effects of procaine on the central nervous system in a nontoxic dose. The yielded results seem to be sufficient to convince us of the variegated central actions of this drug.View full abstractDownload PDF (292K) -
KIKUO OGIU, HIROSHI TAKAGI, MOTOHATSU MATSUMURA, AKIRA YANAI1955 Volume 5 Issue 1 Pages 48-56
Published: 1955
Released on J-STAGE: February 16, 2007
JOURNAL FREE ACCESSIn the previous paper (1), it has been reported that the spinal depressant action which is observed in cats after administration of morphine may be due to a descending inhibitory action mediated through the higher levels. In different species of animals, however, the effect of morphine on the central nervous system is not the same, but is excitatory or depressive as the case may be. Indeed, it is said (2) that morphine has a central excitant action in cats and finally gives rise to a convulsion.
The present experiments have been designed to analyze the relationship between the motor activity and changes of the reflex discharges caused by sciatic stimulation associated with the administration of higher doses of morphine.View full abstractDownload PDF (522K) -
HIROAKI KUROSE1955 Volume 5 Issue 1 Pages 57-65
Published: 1955
Released on J-STAGE: February 16, 2007
JOURNAL FREE ACCESSThere are many studies concerning the cumulative effect of digitalis glycosides. Of old, Fraenkel (1) observed their cumulative effect in cats by the consecutive administration, and Gottlieb (2), Takayanagi (3), Hesse et al. (4) and Lendle (5) investigated the effect in frogs by the same way. Besides these, the experimental studies have been made by using a variety of methods in dogs, rabbits, pigeons and mice.
In experiments on frogs, Takayanagi injected the cardiac glycosides for several days together and measured the total dose required to cause intoxication and the additional lethal dose of the drugs after the continuous infusion. Of late, Teodoru and Branceni (6) measured, first, the time needed for the cardiac glycosides to produce their effect by means of the perfusion method of the in vivo heart of frogs, and next, the time required for them to be washed away with the Ringer's solution, and then estimated an amount of the drugs accumulated.
In those experiments, the amount of drugs is estimated mainly from the total lethal dose or the additional dose necessary for the occurrence of the lethal effect on the presumption that drugs would be stored intact in the cardiac muscle. But various questions are cast to this procedure, and at present, the mechanism of the cumulative action of cardiac glycosides is not clear.
We framed our own plan of experiments with frogs on the assumption that a so called cumulative effect is different substantially between the cold-blooded animal like frogs and the warm-blooded animal such as cats and others, and that drugs may be stored as merely a substance in frogs.. Therefore, we administered first a given amount of cardiac glycosides to frogs, next injected an infusion of the leaves of digitalis purpurea one to ten days later and measured the time elapsed before the appearance of the systolic arrest of the heart in vivo.View full abstractDownload PDF (376K) -
KIRO SHIMAMOTO, OSAMU KANAUCHI, SEIICHI UCHIZUMI1955 Volume 5 Issue 1 Pages 66-76
Published: 1955
Released on J-STAGE: February 16, 2007
JOURNAL FREE ACCESSIt is generally accepted that the ganglion blocking agents such as tetraethylammonium or hexamethonium has scarcely any peripheral action, but tetraethylammonium exhibits a somewhat stronger acetylcholine-like action on the parasympathetic postganglionic effectors than hexamethonium (1). On the other hand, the vasopressor actions of intravenous adrenaline and some other sympathomimetic amines are greatly increased or prolonged after ganglionic transmission is blocked by these agents (2-4). The explanation on this phenomenon differs from each other. As the effects of these agents on some extirpated organs are almost negligible, Paton and Zaimis, and Moe, concluded that this phenomenon derived from the inactivation of the reflex compensatory haemodynamic mechanism. Page and Taylor considered that the phenomenon caused by tetraethylammonium a result of the release of noradrenaline-like substances from the liver. This potentiation occurs also after vagotomy or full atropinization. Therefore it can not result from the blockade of a parasympathetic reflex vasodilatation.
The experiments were directed to analyze further the adrenaline potentiation in other tissues and endeavoured to resolve whether the phenomenon is due to ganglionic. on postganglionic mechanism. The results revealed exactly that the ganglion blocking agents had a definite masked peripheral action beyond the action on the ganglion cells, which modified the response of the sympathetic postganglionic effectors to adrenaline, noradrenaline and the electrical postganglionic nerve stimulation.View full abstractDownload PDF (543K)
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