It is led to the effect that it makes a correlation between physiological change of function and intermediary substance of metabolism, such as acetonuria in case of hunger, increase of pyruvic acid and lactic acid in blood of diabetics as well as avitaminostic stage, and such, which had been made public in effect.
Acute chloroform poisoning (1) and that of many narcotics injure the function of liver and kidney and it was shown by many academic reports of the past that it produces considerable changes in intermediary metabolism. While, Quastel and Wheatly (2) have explained that narcotics inhibit the cerebral cells' oxidation by which a special effect brings about on the various functions. Such being the case, narcotics of each kind are considered to be much correlated in.point of the intermediary run of metabolism.
I tried, therefore, to examine the amount of lactic acid, an intermediate of carbohydrate metabolism, together with acetone, acetoacetic acid and β-hydroxybutyric acid in blood of rabbits, those of fat metabolim, in order to let me know the physiological change of function by giving morphine hydrochloride and soluble phenobarbital.

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It is well known that some of the antihistaminic drug such as diphenhydramine has marked hypnotic action. The mechanism of this action is, however, remained obscure for it acts in experimental animal not as a central depressant but rather as a central stimulant. An attempt was made, therefore, to compare the effect of this drug upon the electroencephalogram (EEG) of man with that of rabbit.

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It is widely known that cocaine potentiates the responses of sympathetically innervated organs to adrenaline, sympathin, and to sympathetic nerve stimulation. Adrenaline potentiating action of cocaine was first observed by Froehlich and Loewi (1) in 1910. But the mode of this action has not yet been clearly established, though many experiments have since been carried out in order to account for the phenomenon. It has been suggested that cocaine enhances the sensitivity of adrenergic effector systems, or protects the autoxidation of adrenaline or increases the permeability of sympathetically innervated cells, , thus favoring the entrance of stimulating agents. Recently, with the advance in the study of metabolism of adrenaline, it has been suggested that the potentiating action of cocaine is due to inhibition of the enzymatic systems which inactivate adrenaline in vivo.
On the other hand, the fate of adrenaline Is still unknown, in spite of many experiments that have been done on this problem. Hynal (2) and many others reported that liver destroys adrenaline in vivo, while Markowitz (3) and others obtained the negative results. Even in vitro experiments, Embden (4) and others observed the destruction of adrenaline in blood but Machii (5) and others observed the fact that adrenaline is inactivated by perfusion through the isolated liver or other organs, or by addition o:f various tissue extracts. On the contrary, Oliver and Schaefer (6) found that small amount of suprarenal extract or adrenaline retained its activity much longer in blood than in aqueous solution, and this observation has many times been confirmed by Wiltshire (7) and many other investigators who suggested that in blood and tissues is present an inhibitor of autoxidation of adrenaline such as protein, amino acids, ascorbic acid or glutathion.
More recently, various enzymes inactivating adrenaline were discovered from animal and plant tissues and one of them is called amine oxidase. It is considered that amine oxidase is contained abundantly in liver and intestine, the inactivating power of which is much stronger than that in other organs. It is not yet clear, however, how much important part these enzymes play in the inactivation of adrenaline in the animal body. Richter (8) reported that the rapid inactivation of adrenaline in vivo is rather due to sulfoconjugation than to amine oxidase. Bacq (9) has also expressed doubts on the deamination of adrenaline due to amineoxidase in vivo. Okamura (10) described that the rapid disappearance of the biological action of adrenaline in vivo is mainly due to the adsorption of adrenaline by red blood-corpuscles but not due to the oxidative destruction.
Since Gaddum (11) has explained the ephedrine potentiation to adrenaline by inhibition of amine oxidase, MacGregor (12), Tripot (13) and Philpot (14) have extended Gaddum's hypothesis, and have proved that not only ephedrine but also cocaine and other local anesthetics inhibit the action of enzymes which inactivate adrenaline. Philpot (14) pointed out that amine oxidase is much more strongly affected by these local anesthetics than other enzymes, but Bain et al. (15) described that cocaine cannot diminish the adrenaline inactivating power of liver in vitro.
As above mentioned, the fate of adrenaline in vivo is very complicated, and the experimental evidences are not yet sufficient to show how cocaine prevents adrenaline from inactivation. It was, therefore, intended to study the effects of cocaine and other local anesthetics on the action of adrenaline, on the detoxication of adrenaline in liver in vivo and in vitro and also the correlation between blood and tissues (especially liver extract) which may possibly be connected with the inactivation of adrenaline. Furthermore, the influence of local anesthetics (especially cocaine) on the adrenaline inactivation in vitro was investigated.

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Recently methylalcohol is attracting the attention of medical circle, because of many cases of its intoxication, but a lot of questions are still left unanswered as of its pharmacological action. About the distribution of methylalcohol in body and its ways of excretion, there are not so many reports as yet. As far as we know, S. Ueno (1) analysed the methylalcohol contents of various organs of corpses by its intoxication and found that most methylalcohol was contained in blood, and then came out in order of urine, bile, brain and stomach contents. A. Benedicenti (2) let the cats inhale methylalcohol of 3, 4 vol.% eight hours long, and recovered it in the organs as follows : blood, 0, 562g %; liver 0.207; brain 0.19; urine 0.528. According to M. Nicloux (3) and M. Neymark (4), methylalcohol remains in body longer than ethylalcohol. We made the same analysis systematically on more organs than they did.

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At the present time, ascariasis is to be considered as one of the serious medical problems in the oriental countries including Japan. In many human experiments in our country, it is found that both santonin and hexylresorcinol are reliable in their anthelminthic action (1). From the result of comparable studies on the pharmacological as well as clinical benefits of both drugs, it is confirmed that santonin is markedly superior to the other in view of its negligible side action. Effective doses of santonin never induce ill effects except a slight and temporary disturbance in vision, while oral administration of hexylresorcinol induced some local irritations on the mucous membrane of the digestive organ, even when it was administered under a perfect condition of coating on it. After taking santonin, ascaris are expelled alive and active. Some authorities, therefore, assume that santonin is not directly toxic to the parasites, but that rather they are irritated by the drug and migrate from the small intestine to the colon to be expelled (2-6). According to others, the drug is excreted in the intestine as an unknown compound, possibly an oxidation product, on which the ascaricidal properties may depend (7-12). But there has been no positive evidence to support both of the views until recently. We have now been able to find out a characteristic locomotion of ascaris in a glass tube which is made to imitate the shape of the bowel, and have good reasons to connect this movement of the worm closely with the anthelminthic activity of santonin (13).

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