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Intra‐arterial injections of substance P in doses from 10 to 30 units potentiated the response of the nictitating membrane to submaximal stimulation of the preganglionic sympathetic nerve, while higher doses (30 to 100 units) usually depressed the response. The stimulating action of acetylcholine on the superior cervical ganglion (as judged by the response of the nictitating membrane) was also potentiated by substance P. The responses of the nictitating membrane to adrenaline, noradrenaline and tyramine were potentiated by substance P as well. It is concluded that the potentiating effect of substance P on the response of the nictitating membrane to sub‐maximal stimulation of the preganglionic sympathetic nerve is probably due to sensitization of acetylcholine receptors in the postsynaptic neurone. The present experiments do not explain how substance P potentiated the response to sympathomimetic amines. 1960 British Pharmacological Society

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Several factors influencing the hypertensive effect of eserine in the rat were investigated. Pretreatment with reserpine regularly depressed or abolished the hypertensive response to eserine. The slow intravenous infusion of either noradrenaline, dihydroxyphenylalanine or 5‐hydroxytryptamine only occasionally restored the hypertensive effect of eserine in reserpine‐treated rats. Bretylium and choline 2,6‐xylyl ether bromide significantly depressed or even abolished the hypertensive effect of eserine. The effect of bretylium was stronger than that of choline 2,6‐xylyl ether bromide. Cocaine was found to antagonize the action of bretylium on the response to eserine. In doses which significantly depressed the action of eserine bretylium did not inhibit the hypertension due to excitation of medullary centres induced by clamping the common carotid arteries. Lowering of body temperature abolished the hypertensive effect of eserine. Pretreatment with isopropylisoniazid did not antagonize the inhibitory action of reserpine on the hypertensive response to eserine. It is concluded that the present experiments indicate that the hypertensive effect of eserine in the rat is due to central activation of adrenergic nervous elements. Liberation of noradrenaline (and adrenaline) from the adrenals and from the blood vessels by eserine is an insignificant factor in producing the hypertensive response to eserine. 1961 British Pharmacological Society

Tyramine is mainly a pressor agent in the rat under urethane, although the hypertensive effect of tyramine in some experiments is followed by a prolonged increase or depression of blood pressure. Bretylium, in doses up to 10 mg/kg, prolonged the response to tyramine, whereas larger doses depressed or blocked its effect. When the hypertensive effect of tyramine was blocked by bretylium, both noradrenaline and dihydroxyphenylalanine, when slowly infused, were found to restore it. The well‐known block by cocaine of the hypertensive response to tyramine could also be reversed by intravenous infusion of noradrenaline and dihydroxyphenylalanine. It is concluded that the infusion of noradrenaline and dihydroxyphenylalanine makes available noradrenaline in the postganglionic adrenergic nerves which is necessary for the action of tyramine. 1961 British Pharmacological Society

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Guanethidine, hemicholinium and mebutamate were used to study the site and mechanism of the hypertensive response to eserine in the rat. Guanethidine was found to block very effectively the hypertensive effect of eserine and to produce at the same time a very strong potentiation of the response to catechol amines. Hemicholinium, after a certain latent period, also blocked the effect of eserine, at the same time leaving the response to adrenaline and noradrenaline intact. Mebutamate was also found to block the effect of eserine. The results of the present experiments suggest that eserine produces a central adrenergic activation in the rat. 1962 British Pharmacological Society

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Examination of patients with different degrees of hearing loss or deafness in areas of endemic goitre has shown that more than half of the number had radiologic evidence of platybasia. The same could be found in cretins from these areas during clinical studies. Some of the findings are shown and compared with the radiological analysis of fetal skulls with physiological platybasia. These findings give strength to the assumption that a retardation in the development of the central nervous system has taken place early in fetal life as a result of the hypofunction of the fetal thyroid gland. © 1963 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted.

After intracerebral injection in mice, the analgesic effect of morphine depended on the dose. Two phenylacetic acid esters, CFT 1201 (diethylaminoethylphenyldiallyl acetate) and CFT 1208 (diethylaminoethylphenylallyl acetate), injected intraperitoneally, potentiated the analgesic action of 0·5 μg. of morphine, injected into the posterior portion of the brain 90 min. later. When the phenyl acetates were injected (50 μg.) into the brain, they potentiated the analgesic action of morphine, injected subcutaneously (10 mg./kg.) 80 min. later. The results show that the inhibitors of the hepatic microsomal enzymes may affect the action of analgesics by an action on the central nervous system. 1963 Royal Pharmaceutical Society of Great Britain

The actions of α‐methyl‐m‐tyrosine (mmt) and reserpine upon the analgesic effect of morphine has been studied in rats and mice. In rats, reserpine antagonised the effect of morphine, while mmt did not cause any appreciable change of the effect of morphine, injected either 2 or 24 hr after mmt. Reserpine also produced its antagonistic action to morphine in rats which were previously (24 hr) treated with mmt. Both mmt and reserpine potentiated the effect of morphine in rats pretreated (24 hr previously) with iproniazid. In mice, both mmt and reserpine antagonised the effect of morphine. Reserpine failed to do so in mmt pretreated animals. The effect of morphine was restored 24 hr after the injection of mmt. It is suggested that the inhibitory action of reserpine upon the analgesic effect of morphine is due to the antagonistic action of brain 5‐ht, which is activated after being released from its stores by reserpine. The pattern of reserpine—mmt—morphine interactions in rats probably differs from that in mice. 1964 Royal Pharmaceutical Society of Great Britain

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