Allium sativum (Garlic) is a cultivated vegetable. Al-Rawi and Chakravarty (1) indicated the therapeutic use of the bulb and juice of this plant. Actually the bulb is used in various forms of ulcers and regulation of the menstrual cycle. The juice is also used as a rubefacient in skin diseases and external ottitis and as a lotion for washing the wounds and ulcers. In addition to the wind-breaking and helminthic effect, the juice showed an improvement of the urinary secretion and sweating and an antipyretic effect in the patient with an intermittent fever. Thus, the main therapeutic indications of the juice as a syrup are diaphoretic, diuretic and expectorant effects. Inspite of the wide therapeutic availability, the biological activity of this plant is little known. Therefore, in the present experiments the effects of water and alcohol extracts of Allium sativum on the various organ functions were observed.

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The activities of drug-metabolizing enzymes of rat liver microsomes were altered by some unphysiological conditions (1-7). In previous papers we reported that the activities of hexobarbital hydroxylase and aminopyrine N-demethylase, which showed clear sex difference, were markedly decreased in the thyroxine treated male rats, whereas in female rats these activities were increased and the activity of aniline hydroxylase, which showed no clear sex difference, was increased in both male and female (3, 6). Similar results as observed in normal rats were obtained in male and female rats gonadectomized and treated with androgenic or anabolic hormones (3). These results, thus, indicate that the activities of hexobarbital hydroxylase and aminopyrine N-demethylase are dependent upon the anabolic action of male sex hormone and thyroxine probably decreases the androgen stimulated activity (3, 6).
On the other hand, it has been supposed that the androgen-dependent regulation mechanism of microsomal drug-metabolizing activity is likely present only in rats, but it is lack in other species of animals (8-10). Thus, it is of interest to investigate whether or not the sex difference in the effect of thyroxine on the drug-metabolizing enzymes is only observed in rats and the effect of thyroxine in other species of male and female is similar to that observed in female rats. The possibility of this assumption was investigated with both male and female rats, mice and rabbits and reported in the present paper. Moreover, since the activity of drug-metabolizing enzymes was connected with the activity of NADPH-linked electron transport system of liver microsomes, the correlation of both activities under the thyroxine treatment was also investigated (4-7, 11-15).

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It was reported earlier (1) that cyproheptadine possesses marked antiarrhythmic action against both atrial and ventricular arrhythmias. Since BC 105 is closely related to cyproheptadine (Periactine) differing only in the substitution of a thiophene nucleus for a benzene nucleus (2), it was taken up for study to see whether this compound also has antiarrhythmic property or not. The present paper deals with the evaluation of antiarrhythmic property of this compound. BC 105 is the malate of 4-(l-methyl-piperidylinene-4)-9, 10-dihydro-4H-benzo (4, 5) cyclohepta (1, 2-b) thiophen.

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Various drugs are inactivated by liver microsomes in the presence of NADPH and atomospheric oxygen (1). The enzymes catalyzing these reactions can activate molecular oxygen by a two-electron reduction so that one oxygen atom is introduced into the substrate leading to a hydroxylated product, whereas the second atom is reduced to water (1, 2).
Recently the participation in these reactions of hemoprotein called cytochrome P-450 (3) as the oxygen-activating component (4-8) has been established (Fig. 1).
The activity of drug-metabolizing enzymes of liver microsomes was altered by various factors, such as the administration of phenobarbital or methylcholanthrene (9, 10), thyroxine (11-13), anabolic hormone (11, 14, 15), carbon tetrachloride (11, 16) and morphine (11, 12), and adrenalectomy (11, 17), thyroidectomy (13), hepatectomy (18), starvation (19, 20), alloxan diabetes (11, 12) and low protein diet (16, 21, 22).
It was also demonstrated that the activity of NADPH-linked electron transport system of liver microsomes was often altered in association with the alteration in the activity of drug-metabolizing enzymes under the above-given conditions (10, 13, 22, 26).
Vitamin C is a well known component related to the control of oxido-reduction states of living cell, but detailed role of vitamin C has not been fully elucidated (27). On the other hand, Mitoma et al. (28), Tochino et al. (29) and more recently, Conney et al. (30) reported that the hydroxylation of acetanilide, hexobarbital and zoxazolamine was decreased in vitamin C deficient guinea-pigs.
However, the studies on the mechanism of decreased hydroxylation activity in relation to the activity of NADPH-linked electron transport system has not yet been reported. The purpose of the present study, therefore, is to investigate whether or not the mechanism of decreased hydroxylation activity of liver microsomes from vitamin C deficient guinea-pigs is related to the decreased activity of NADPH-linked electron transport system.

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Vor kurzem wurde eine Gruppe von 4-oxy-phenyl-l-isopropanol-phenyl-iso-butylamin Derivaten (Nilidrin) (Tab. 1) synthetisiert (1), bei denen das H des Phenoloxydrils in Position 4 and das H des Alkoholoxydrils des β-Carboniums des Isopropanols ersetzt wird.
Wegen der strukturellen Analogie, die zwischen Isoprenalin, Isoetharin, Protochylol, Dichloroisoprenalin, Pronethalol, Propranolol, usw, and auf der anderen Seite zwischen Isoxuprin, Nilidrin and den kilrzlich synthetisierten Derivaten dieser Substanz, die wir oben erwähnten, besteht, und, in Betracht ziehend, class man Nilidrin, neben der prädominierenden myolytischen Wirkung auch manchmal stimulierende Wirkungen auf die β-Rezeptoren und manchmal deprimierende Wirkungen auf die α-Rezeptoren zuschreibt (2, 3), erschien es uns interessant, die eventuellen deprimierenden oder stimulierenden Wirkungen der kürzlich synthetisierten Derivate auf die adrenergischen α- und β-Rezeptoren zu untersuchen, und, wenn möglich, Zusammenhänge zwischen den Veränderungen der chemischen Struktur und den pharmakodynamischen Veränderungen hinsichtlich dieser Rezeptoren, festzustellen.

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The administration of phenobarbital markedly increased the activities of drug-metabolizing enzymes and NADPH-linked electron transport system of liver microsomes (1-4). Moreover, the administration of phenobarbital increased the amount of liver microsomal protein and the incorporation of amino acid into liver microsomal protein (5, 6).
The effects of phenobarbital to induce the activities of drug-metabolizing enzymes in tumor-bearing rats and immature rats were higher than those in normal rats and mature rats (7, 8).
These results suggest that the effect of phenobarbital to induce the activities of drug-metabolizing enzymes may be related to the rate of biosynthesis of protein in liver microsomes.
In a previous paper, it was reported that the activities of drug-metabolizing enzymes in alloxan diabetic and thyroxine-treated male rats were decreased, while the same activities in female rats were slightly increased. The decrease in the activities in male rats seemed to be due to an interference in the androgen-dependent stimulation (9).
It is well known that the incorporation of amino acid into liver microsomal protein is decreased in alloxan diabetic rats, while the incorporation is increased in thyroxinetreated rats (10-12).
Thus, the purpose of present studies was to investigate whether the effect of phenobarbital to induce the activities of drug-metabolizing enzymes and NADPH-linked electron transport system is increased in thyroxine-treated rats and decreased in alloxan diabetic rats.

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Various foreign compounds were oxidized in liver microsomes by so-called “microsomal drug-metabolizing enzymes” under the presence of NADPH and atmospheric oxygen (1).
The enzymes catalyzing these reactions can activate molecular oxygen by two-electron reduction so that one oxygen atom is introduced into the substrate leading to a hydroxylated product, whereas the second atom is reduced to water.
Since microsomal cytochrome P-450 is involved in the oxidation of drugs, the following tentative pathway has been postulated (2-4) (Fig. 1).
It is well known that one of the characteristic of these enzyme systems is a low substrate specificity and indeed highly lipid-soluble compounds were metabolized by these enzyme systems (1). These reactions including hydroxylation of alkyl side-chain, hydroxylation of aromatic and non-aromatic rings, N-dealkylation, O-dealkylation, sulfoxidation and N-oxidation. However, it is not yet determined whether or not cytochrome P-450 acts as only an oxygen-activated component and the terminal oxidase is required for the oxidation of drugs. In other words, it is not clear whether or not activated oxygen of cytochrome P-450 is transfered non-enzymatically into drug molecule.
In the present communication, we wish to report the evidence which may suggest the presence of the terminal oxidase and moreover the presence of more than two kinds of hydroxylase and N-demethylase.
The results indicate that the terminal oxidase which hydroxylates pentobarbital and hexobarbital is likely differ from that which hydroxylates aniline and zoxazolamine for the following reasons: the presence of marked sex difference in the activity, the difference in the effect of methylcholanthrene and some inhibitors, such as SKF 525A and DPEA and the difference in the enzyme stability (1, 6, 7).
Similarly, the terminal oxidase which N-demethylates aminopyrine is likely differ from that N-demethylates N-methylaniline.

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Writing is a motor act which is acquired early in life and the performance thereafter remains stable over long periods of time in adult individuals. Successive samples are, thus unlikely to be affected by further practice (1). At the same time, handwriting, being a complex motor act requiring fine co-ordination should be more sensitive to the effects of psychoactive agents than simple skills (2). Further, repeated samples of handwriting can be obtained easily and quickly.
In the present investigation effects of four psychoactive agents, caffeine, chlorpromazinc, methamphetamine and phenobarbitone, on handwriting have been studied. A preliminary report of the work has appeared (3).

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Although noradrenaline (NA) is well known for its pressor effect, it has been shown to produce a depressor response in hypothermic cats and dogs (1, 2) ; the mechanism of the latter effect has, however, not yet been clearly elucidated. This effect has been attributed to its ganglion blocking action (1) as well as to the parasympathetic over-activity resulting from the altered state of the higher autonomic center during hypothermia (2). It was, therefore, the object of this study to investigate further the mechanism of this depressor response to NA during hypothermia.

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It has been generally known that feeding rats the low protein diet results in an accumulation of lipids in the liver. Fatty livers of rats caused by the imbalance of amino acids in the body were reported to be produced by excessive or deficient sulfur-containing amino acids (1, 2) as well as by deficient lysine and threonine in the diet (3). It was reported by Ashida that the extent of lipid accumulation in the liver of rats was more marked with albumin than with casein as a dietary source of protein, and that the increase of sulfur-containing amino acids content in the low protein diet activates the development of fatty liver (2). Moreover, he showed that the variation in the mixing ratio of methionine and cystine in the artificial low protein diet did not significantly affect the extent of the hepatic neutral fat.
Methionine and cysteine are precursor amino acids for the physiological synthesis of coenzyme A in the mammalian species.
Since coenzyme A correlates essentially the metabolic process of carbohydrates, protein, fat and steroid substances as well as the detoxication mechanism including the acetylation, effects of the agents relating to the endogenous formation of coenzyme A on the hepatic lipids accumulation were studied in this experiment.
In the present experiments a fatty liver was produced by feeding rats the low protein diet in an attempts to know the possible development of fatty livers caused by the imbalance of amino acids, to compare the prophylactic and therapeutic effects of pantethine, calcium pantothenate, methionine and cysteine on the fatty liver and to establish some correlation, if possible, between the activity of coenzyme A and the level of lipid in the liver.

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The biphasic mode of action of gamma-butyrolactone (GBL) and gamma-hydroxybutyrate (GHB) in the central nervous system has been confirmed in the previous report (1). The former compound elevates the reticular arousal stimulation threshold for the manifestation of the hippocampal theta waves without significantly affecting the increased manifestation of the fast waves in the rabbit's EEG. At the same time, the thalamic recruiting response is usually depressed or sometimes is slightly augmented. In order to observe the mode of action on the brain structures more in detail, the effects of both compounds on the cortical dendritic responses (DR) caused by the electrical stimulation of the cortical surface are studied in the cats.
The small doses of GHB augment the DR, while the large doses inhibit it. Based on the obtained results the dose-response relationship of GHB and its related compounds is discussed. On the other hand, GBL proved to be inactive in this respect. Correlation of the effects between GHB and gamma-aminobutyric acid (GABA), the latter of which is now accepted as the inhibitory transmitter in the several parts of the central nervous system, is also investigated. Roth et al. (2, 3) have already postulated that GHB is the pharmacologically active metabolite derived from gamma-butyrolactone in the body.

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In the previous paper (1), the author reported that the intraventricular administration of adrenaline induced both the arousal and the restng pattern of EEG in rabbits, and that the intraventricular pretreatment of alpha-adrenergic blocking agents suppressed the appearance of the resting pattern, while the resting or sleep pattern appeared more markedly following the pretreatment with beta-adrenergic blocking agents. These results suggest that the EEG resting pattern induced by the intraventricular administration of adrenaline may be dependent on its alpha action, and that there may be two contrasting effects on EEG depending on the alpha and the beta action of the catecholamine injected intraventricularly. In the present experiment, the author reevaluated these hypotheses by examining effects of the intraventricular administration of noradrenaline, phenylephrine and isoproterenol on rabbit's EEG. Modifications of the effects of intraventricularly administered adrenaline were also studied following the systemic pretreatment of dibenamine or reserpine.

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Supersensitivity to catecholamines in various organs after reserpine treatment has been reported by many investigators. Trendelenburg et al. (1) described that this action was associated with the impairment of uptake of catecholamines to adrenergic nerve terminals. On the other hand isoproterenol, one of the catecholamines, was not retained by the heart (2). Neither cocaine (3) nor denervation (4) could cause supersensitivity to this amine.
However, Fleming et al. (5) reported that after reserpine treatment the isolated ileum of rabbit became more sensitive to isoproterenol and recently Khan et al. (6) also showed that on the isolated rat fundus strip preparation reserpine and guanethidine increased the sensitivity to isoproterenol. But further evidences for these phenomena were not obtained.
In a previous paper (7) authors reported briefly that on the blood pressure of the rat treated with reserpine the hypotensive action of isoproterenol was potentiated. In order to confirm our previous results, the effects of reserpine on the sensitivity to isoproterenol and a new adrenergic β-stimulating agent trimethoquinol (8) were studied on the blood pressure of the rat.

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Studies on the antitussive agents have been advanced with the development of bioassay for them. At the present time, a large number of non-narcotic synthetic antitussives are employed in the management of cough instead of narcotic antitussives.
The evaluation method for antitussive activity was first reported by Ernst in 1938 (1), that is, coughing was induced by pinching the trachea of a cat which had previously been made to sero-fibrinous pleurisy by means of intrapleural injection of Lugol solution. Two years later, Eichler and Smiatek (2) reported that coughing could be induced in the guinea pig by an inhalation of aerosolized sulfuric acid. However, these two methods have not been accepted widely for the evaluation of antitussive agents because of uncertainty of cough production. In 1952, Kasée devised two methods (3, 4): 1) electrical stimulation of the superior laryngeal nerve and 2) mechanical stimulation on the tracheal mucosa in the unanesthetized dog. At the same time, Domenjoz (5) reported a method, in which coughs were able to be induced by electric stimulation of the superior laryngeal nerve in the anesthetized cat. Kase as well as Domenjoz insisted that their own methods were suitable for the antitussive evaluation and the results obtained from the animal experiments were in good accordance with clinical effects. Since then, about thirty methods have been presented one after another for the evaluation of antitussive activity. However, they are classified in three groups after all: 1) mechanical stumulation method (3, 4, 6-13), 2) chemical one (2, 6, 8, 10-12, 14-20), and 3) electrical one (3, 5, 21-26).
Anesthesia is used in most of the methods described above. In general, anesthesia has been used as one of routine procedures in animal experiments, but cough reflex is affected by it to a great extent. If anesthesia is an inevitable procedure in the evaluation of antitussives, the influence of anesthesia on antitussive activity should be studied in detail. As far as we know, there has been no report on such study until the present. In the present paper, the influence of anesthesia on antitussive effect was studied in detail and a few remarks necessary for making use of anesthesia in the evaluation of antitussive agents were described.

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The pylorus ligated rat (Shay rat) was described by Shay et al. (1) for the production of acute ulcers in the forestomach, and it has been also employed as a means of studying gastric secretion. This technique is now used extensively as a screening method of gastric secretory depressants and antipeptic ulcer agents (2-4) because of the following advantages: 1) the simplicity of surgical procedure, 2) the high rate and rapid occurrence of ulceration, and 3) the possibility of measurements of gastric secretory rate and severity of ulceration in the same animals; which make up for the shortcoming that ulcers are present only in the forestomach.
The pathogenesis of ulceration in the pylorus ligated rat has been discussed by many investigators, but the definite conclusion is not yet offered. Several factors have been considered as causes of ulceration; such as the digestive effect of gastric juice, the interference of blood circulation or the decrease of mucosal resistance. Sun and Chen (5) concluded that the rumenal ulcers in the pylorus ligated rat might be merely a result of the volume and the concentration of gastric hydrochloric acid and pepsin upon the mucosa. But other factors can not be ruled out completely.
There remains some obscurities also in the gastric secretory mechanism of the pylorus ligated rat. It is often said that the pylorus ligated rat is inadequate for the estimation of stimulants of gastric secretion, for they can hardly increase in gastric secretion in response to stimuli owing to the hypersecretion. The mechanism of the hypersecretion in the pylorus ligated rat is now still controversial.
The present study is an attempt to clarify the effects of various factors on gastric secretory rate and ulceration and to discuss the mechanisms of ulceration and gastric hypersecretion in the pylorus ligated rat.

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In teratological experiments with drugs, the injection by ways of parenteral routes is often used for the advantage of securing certain effects, especially exact dosage-response relation. It has been presumed that the teratogenic action of a drug varies with the mode of parenteral administration, even if the same total daily dosage is employed and this may be due to the variations in the nature of metabolites of a drug and their concentration or duration in the embryonic tissues. There is little information in this area at hand. Isaacson and Chaudhry (1) reported that the incidence of cortisone-induced cleft palate in mouse embryos is higher when administration of 4 small doses at 6-hour interval is given rather than a single dose of the total amount.
The teratogenicity of caffeine in mice was established and some of its mechanisms were studied by our group (2-4). The rapid metabolic rate and no apparent accumulation in the body of this compound established in man (5) can be presumably applied to other mammals. So the administration of caffeine could be an advantageous tool for analytical studies of teratogenicity in experimental mammals. This study was undertaken to establish a relationship between teratogenic activity and some modes of administration by using this compound.

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Some studies have been reported on the cation movement in guinea pig's taenia coli in the presence of high concentration of environmental potassium (K) (1-8), none of which has dealt with the effect of high concentration of K on K exchange. In the present study, K exchange has been studied in the guinea pig's taenia coli under elevated environmental K concentration for the purpose of clarifying the physiological nature of K-induced contracture, following the previous mechanographic study of the same purpose (9).

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Mechanism as to the positive inotropic action of cardiac glycosides at the cellular level is still a matter of speculation. It could, however, be said that the high energy phosphates which are involved in energy production, do not appear to be implicated in the action of the glycosides (1-3). Action of the glycosides on electrolyte exchange process has been intensively investigated. But a therapeutic effect of ouabain has been shown to occur without any changes in transmembrane- and action potential (4-6). Therefore, the possibility that the positive inotropic action takes place on the basis of change in sodium and/or potassium metabolism appears to be also unlikely. Nayler pointed out in her recent review (7) that the most interesting findings on electrolyte and the glycosides would be those on calcium. Many recent reports (8-10) suggest an intimate relationship between the glycosides action and intracellular calcium, which takes an essential part in the activation and the maintenance of the contractile process (11, 12).
Kuffler and Huxley (13, 14) reported that the first step in the process of muscular contraction is the depolarization of excitable membrane; therefore, twitch and potassium contracture are essentially the same with respect to initiation of the contractile process. Thus, the first series of events in the production of both responses consists of depolarization and the following initiation of linking process, through which ionized calcium is released within cell. Hodgkin and Horowicz (15) examined precisely the relation between contractile tension development and the change in the membrane potential given by various external potassium concentrations and determined a mechanical threshold of membrane potential for initiation of contractile apparatus. Otsuka and Nonomura (16) studied the influence of ouabain on such a relation between membrane potential and contractile tension development in the frog heart and showed that the cardiac glycoside alters the relation so that a smaller depolarization is required for the development of a given tension.
Our attention was paid to the findings. In the present report, a series of such an experiment has been, done, and that in the presence of various steroid hormones: because, several reports showed that some mineralocorticoids have anti-ouabain action on ion-transport of human erythrocyte (17), contraction of rat aortic strip (18) and potassium out-flux of guinea pig heart (19). In the first series of present study, anti-ouabain action of aldosterone on both twitch and potassium-induced contracture and on the relation between membrane potential and developed tension was investigated in frog heart. Then, anti-ouabain action of other corticoids and some sexual hormones was studied and anti-ouabain potency of these steroid hormones was compared to that of aldosterone. Results obtained demonstrate that the corticoids tested and some sexual hormones can inhibit the positive inotropic action of ouabain so that the shift of mechanical threshold of membrane potential by ouabain is cancelled partially or almost completely by these steroid hormones.

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Lactose exists only in milk as a product of the mammary gland and its considerable amount is found in the milk of many animals except in that of ocean animals, such as whales and seals (1). Lactose is suggested to play an important role for the biosynthesis of galactocerebroside (2-4) (Fig. 1).
On the other hand, lactose added to milk has an undesirable character. First, there are many reports on sucklings about the addition of lactose to the milk being deleterious. Second, many clinicians have experimented with congenital or acquired intolerances for lactose ingestion. Third, it has been reported by Tamura (5) that dyspepsia with diarrhoea in suckling is induced by the accumulation of galactose-l-phosphate, the inhibition of lactose activity in the intestinal wall and an acceleration of permeability of the intestine.
Riggs and Beaty (6) reported that animals, which are fed on a hyper-lactose diet, are arrested in their growth, and some disorder of the intestine, especially diarrhoea, occurs in mammalians and birds. Mitchell and Day (8) found that the cataract occurs in the rat. Takuma and Takayama (9) and Tamura and Ogihara (10) also observed that cataract and a disorder of nutrition of rat caused by lactose are prevented by an addition of whey in the diet (Fig. 2).
The metabolism of lactose mentioned by Bihler and Crane (11) is as follows: lactose was decomposed to galactose and lactose, and turned in cytoplasma with sodium ion. Then, glucose was availed in glycolytic or non-glycolytic metabolism, and galactose was metabolized through the Leloir enzyme system (1) (Fig. 3).
Now, we can take the view that the inhibition of enzymes occurred in the Leloir way in the above-mentioned disease of sucklings and rats. The authors studied the activity of the Leloir enzyme system in rats fed on a hyperlactose or a hypergalactose diet, and the effect of whey including the promoting factor of lactose or galactose metabolism upon this system.

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Mitchell and Dodge (1) have already reported that cataracts broke out in rats fed on a diet containing hyper-lactose, and thus lactose and galactose would be recognized as the factors inducing the cataracts. On the other hand, there were some investigations that cataracts in rats were inhibited by whey. Takuma and Takayama (2) confirmed that a cataract caused by purified lactose was prevented by the addition of whey. Moreover, Ogihara (3) extracted an agent preventing cataract in the whey. Lerman (4) and Schwarz and Golberg (5) noted that the concentration of galactose-l-phosphate(Gal-l-P) in the lenses of cataract-rats caused by an excess of galactose was approximately ten times as thick as is in the normal rat's lenses. Since the metabolism of the lens is dependent upon glucose as its main source of energy, an accumulation of Gal-l-P in the lens may be a promoting factor in the development of the experimental galactose cataract. It has been shown that an excess of Gal-l-P induces a depression of the hexose monophosphate shunt in the lenses (6, 7). This finding supported other reports (8-10) of a depressed activity of D-glucose-6-phosphate: NADP oxidoreductase (1.1.1.49) in the lenses, measured under the same conditions. Korc investigated that the activity of D-glucose-6-phosphate: NADP oxidoreductase of erythrocyte and liver was more accelerated in the rats fed on the galactose diet than in normal rats.
As shown in the investigations mentioned above, these disturbances of galactose metabolism may be the cause of such cataracts.
There are many reports concerning changes of electrolyte concentration in the rat's lenses caused by a diet containing an excess of lactose or galactose. Salit, Swan and Paul (11) and Hill and Heggeness (12) observed that there was a high concentration of sodium and calcium and a low concentration of potassium.
In the present investigations, the authors tried to ascertain the activity of D-glucose-6-phosphate: NADP oxidoreductase (1.1.1.49) in the eye-ball and erythrocyte and changes of electrolytes in the eye-balls in rats fed on a diet containing an excess of lactose and galactose. Moreover, the authors tried to show the effects of the promoting factors of lactose and galactose metabolism in the whey upon this enzyme system and the -changes of electrolytes.

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