Summary1. Intraperitoneal injection of graded doses of ketamine produced a dosedependent fall in body temperature of rats. Similarly, intracerebral injection of much smaller doses produced hypothermia. 2. Pretreatment of the rats with p-chlorophenylalanine (PCPA) greatly attenuated the hypothermic response to ketamine whereas the intraperitoneal injection of 5-hydroxytryptophan in PCPA-treated rats restored the hypothermic effect of ketamine. 3. Depletion of the brain monoamines by reserpine completely prevented the ketamine-induced hypothermia. Treatment with sodium diethyldithiocarbamate (DEDTC), however, did not modify the hypothermic effect of ketamine. 4. Pretreatment of the rats with pargyline potentiated the ketamine-induced hypothermia. 5. Depletion of brain monoamines by reserpine in combination with inhibition of noradrenaline biosynthesis (DEDTC) resulted in a long lasting fall in temperature which was not modified by ketamine. 6. When the ambient temperature was raised from 260 C to 320 C, ketamineinduced hypothermia was much reduced and superimposed on a hyperthermia which occurred in all animals. 7. It is concluded that ketamine produces hypothermia in rats possibly through the release of 5-hydroxytryptamine in the hypothalamus and that this effect is similar in some respects to that produced by morphine in non-tolerant rats.
Summary Inhibition of 5‐hydroxytryptamine (5‐HT) synthesis by p‐chlorphenylalanine protected rabbits pretreated with pargyline from the fatal hyperthermic reaction which occurs on the intravenous injection of pethidine. The development of tolerance to morphine did not protect against the fatal pargyline‐pethidine hyperpyrexia. Moreover, the injection of nalorphine before or after pethidine conferred no protection. Pethidine evoked a hyperpyrexia in rabbits pretreated with lithium sulphate or yohimbine. Sodium diethyldithiocarbamate caused a fatal hyperpyrexia in rabbits pretreated with pargyline. It is concluded that the pargyline‐pethidine hyperthermic interaction might involve the relative concentrations of 5‐HT and noradrenaline in the hypothalamus.
The results obtained from the measurement of the 5-hydroxytryptamine (5HT) content of mouse tissue during pregnancy (Robson & Senior, 1964) led us to undertake a similar investigation in the rat. Dixon (1959) measured the 5HT level in rat foetuses, and found that it reached a peak on the first day after birth, after rising steadily from about the fifteenth day of gestation.Several workers (Nachmias, 1960;Karki, Kuntzman & Brodie, 1962) have investigated the level of 5HT in the brain of the newborn rat, and have found it to be about one-third of that found in the adult rat brain. Nachmias (1960) also showed that the amount of amine oxidase in the rat brain at birth was much lower than in the adult brain.In the current experiments the levels of 5HT in the placenta and foetus have been measured in the second half of pregnancy, as have some of the levels in other maternal tissues. In an attempt to account for the amount of 5HT found in the untreated placenta, the maternal blood content of the placenta in the latter half of pregnancy was measured, and this was correlated with the maternal blood level of 5HT. Following the findings by Correll, Lyth, Long & Vanderpoel (1952) and Waugh & Pearl (1960) that 5HT produced deleterious effects on pregnancy in the rat, the level of 5HT was measured in the placenta and foetus after the administration of this drug. As 5HT treatment of the mother caused a rise in the 5HT level of the placenta it seemed of interest to investigate the effect of monoamine oxidase inhibitors, particularly as these substances had failed to change the level of 5HT in the mouse placenta (Robson & Senior, 1964). METHODSThe experiments were performed on mature Wistar albino rats, weighing 250 to 400 g. They were housed in the Animal House, Guy's Hospital Medical School, and allowed food and water ad libitum. The food consisted of rat cake obtained from the North East Agricultural Society, Aberdeen. The pregnancy was dated by finding spermatazoa in the vaginal smear. The animal was then isolated from the male and pregnancy was confirmed from the 12th day onward by palpation.
Summary Pure khellinin, m.pt. 175° to 176°C., possesses a persistent, rather selective stimulant action on the heart producing a more complete systole and a more complete diastole with a corresponding increase in cardiac output. It raises blood pressure. The glycoside is active and doses of 1 to 1ṁ5 mg./kg. of dog by intravenous injection. It increases the coronary flow, and is non-cumulative. Pure visammin, m.pt. 153° to 154°C., depresses the heart, producing principally a less complete systole with diminished cardiac output. The drug is active in doses of 2 to 4 mg./kg. of dog by intravenous injection. It increases the coronary flow. The impurities present in crude samples of khellinin or of visammin influence to an appreciable degree the normal response of the heart to the pure products.
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