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Biomedical subjects

W Feldberg

Publications and source records attributed to W Feldberg.

At least 91 records · Page 5Linked to original sources
PubMed1968

Temperature effects of reserpine injected into the cerebral ventricles of rabbits and cats.

1. In unanaesthetized rabbits and cats reserpine was injected through a chronically implanted cannula in the left lateral cerebral ventricle, and rectal temperature was recorded.2. In rabbits the reserpine (0.5-0.6 mg) caused a rise in temperature, frequent defaecation and sedation. On repeating the intraventricular injections at 24 hr intervals the rise in temperature was not obtained with the second or third injection, but defaecation and sedation still occurred. When the hyperthermic response to intraventricular reserpine had disappeared the anterior hypothalamus still responded to intraventricular noradrenaline which produced a rise in temperature.3. In cats the reserpine (0.5-0.75 mg) caused a biphasic change in temperature, i.e. an initial fall followed by a rise, frequent defaecation, and catalepsy. On repeating the intraventricular injections at 24 hr intervals the initial hypothermic phase of the temperature response was not obtained with the second or third injection, but the late rise, defaecation and catalepsy were still produced. When the hypothermic phase had disappeared the hypothalamus still responded to intraventricular noradrenaline or adrenaline which produced a fall, and to intraventricular 5-hydroxytryptamine (5-HT) which produced a rise in temperature.4. It is concluded that the rise in temperature in rabbits and the initial fall produced in cats is not due to a direct action of reserpine on the cells of the anterior hypothalamus but to noradrenaline released from adrenergic fibres ending at these cells. When these fibres are depleted of their noradrenaline by one or two injections of reserpine, these effects are not obtained because noradrenaline is no longer available to be released in sufficient amounts to raise temperature in rabbits and to lower it in cats.

Animals↗
PubMed1967

Monoamine oxidase inhibition: effect on 5-hydroxytryptamine output from perfused third ventricle and body temperature.

1. In cats anaesthetized with pentobarbitone sodium the third ventricle was perfused with artificial c.s.f., the effluent was collected in 30 min samples and assayed for 5-hydroxytryptamine (5-HT) on the rat stomach-strip preparation. Rectal temperature was monitored continuously.2. On perfusion of artificial c.s.f. through the third ventricle, small amounts of 5-HT appeared in the effluent; the amounts decreased with successive samples.3. When tranylcypromine (Parnate), an inhibitor of amine oxidase, was added to the perfusion fluid and perfusion was continued, the 5-HT output increased. This increase was associated with shivering and a rise in temperature which was not, however, maintained.4. When tranylcypromine was injected intraperitoneally, during the fall in temperature produced by the pentobarbitone sodium anaesthesia, the 5-HT output also increased, shivering occurred and the fall in temperature was halted or reversed. The effect on temperature was maintained.5. When the cat was killed and perfusion was continued, the 5-HT output, already elevated by the tranylcypromine before death, increased even further in the next few samples.

Animals↗
PubMed1967

Body temperature responses in cats and rabbits to the monoamine oxidase inhibitor tranylcypromine.

1. In unanaesthetized cats tranylcypromine (1-10 mg/kg) had scarcely any effect on rectal temperature when injected intraperitoneally, yet such injections prevented the deep and long-lasting fall in rectal temperature which normally occurs when the cat is anaesthetized by intraperitoneal pentobarbitone sodium or intravenous chloralose. The anaesthesia itself, however, was not affected. In some of the experiments with pentobarbitone sodium rectal temperature even rose to fever level.2. In anaesthetized as well as in unanaesthetized cats injections of tranylcypromine (0.1-1 mg) into the cerebral ventricles caused a rise in rectal temperature.3. In rabbits, rectal temperature was scarcely affected when surgical anaesthesia was produced by intravenous infusions of pentobarbitone sodium under the same condition in which, in cats, intraperitoneal pentobarbitone sodium produced a deep and long-lasting fall in temperature, i.e. when no external heat was applied but excessive dissipation of heat was prevented by placing the rabbit on a cotton-wool pad. However, when it was placed on the metal surface of an operating table, the anaesthesia was associated with a deep fall in rectal temperature.5. In anaesthetized and unanaesthetized rabbits tranylcypromine had no effect on rectal temperature when injected intraperitoneally (10 mg/kg) or into the cerebral ventricles (1 mg).5. These results are discussed in relation to the theory that the three monoamines in the hypothalamus, 5-hydroxytryptamine (5-HT), adrenaline and noradrenaline, act as central transmitters in temperature regulation.

Animals↗
PubMed1967

Site of origin of the abnormal discharge in the electrocorticogram produced by tubocurarine perfused through the anterior horn of a lateral ventricle.

1. In cats anaesthetized with chloralose, perfusion of tubocurarine through the anterior horn of a lateral cerebral ventricle produces a rhythmic discharge of high voltage negative spikes recorded from an electrode inserted into this horn. The discharge spreads to the cerebral cortex where it gives rise to synchronous surface negative deflexions of low voltage. They have previously been described as ;slow waves'.2. The discharge results from an excitatory action of tubocurarine on the anterior limbic area, which is a cortical structure in the medial wall of the anterior horn lying rostral to the septum pellucidum.

Animals↗
PubMed1967

Temperature effects produced in dogs and monkeys by injections of monoamines and related substances into the third ventricle.

1. In dogs the effects on rectal temperature of noradrenaline, adrenaline, 5-hydroxytryptamine (5-HT) and of the monoamine oxidase inhibitor tranylcypromine were studied following their injection into the third ventricle through a chronically implanted cannula. Tranylcypromine was given also by the intraperitoneal route.2. The hypothermic effect of the catecholamines and the hyperthermic effect of 5-HT previously demonstrated in anaesthetized dogs were obtained also in an unanaesthetized dog, but 5-HT was effective only in doses under 20 mug.3. Tranylcypromine (1 mg) injected into the third ventricle of dogs anaesthetized with pentobarbitone sodium produced shivering and a rise in temperature.4. Tranylcypromine (10 mg/kg) injected intraperitoneally caused a rise in temperature in the unanaesthetized dog. For a time shivering and panting, two effects which produce opposite change in temperature, were observed together. When injected shortly before an intraperitoneal injection of an anaesthetizing dose of pentobarbitone sodium, tranylcypromine not only prevented the fall in temperature which is normally produced by the anaesthetic but caused a greater and longer lasting rise than when given alone.5. The intraperitoneal injections of tranylcypromine produced profuse salivation, a peripheral effect which persisted after acute denervation and which was not abolished by atropine or tolazoline.6. In rhesus monkeys anaesthetized with intraperitoneal pentobarbitone sodium, noradrenaline, adrenaline, 5-HT and 5-hydroxytryptophan (5-HTP) were injected into the cannulated third ventricle. The catecholamines caused a fall in rectal temperature. No evidence was obtained that the fall resulted from a rise in hypothalamic temperature. The injections of 5-HT or of its precursor 5-HTP raised rectal temperature. Monkeys thus respond to the monoamines injected intraventricularly, in the same way as cats and dogs, and unlike rabbits, sheep, goats, oxen and rats.

Animals↗
PubMed1966

Appearance of 5-hydroxytryptamine and an unidentified pharmacologically active lipid acid in effluent from perfused cerebral ventricles.

1. In cats anaesthetized with intraperitoneal pentobarbitone sodium, three regions of the cerebral ventricles, the third ventricle, the inferior or the anterior horn, were perfused with artificial c.s.f. and the effluent was tested on the fundus strip of the rat's stomach.2. Effluent from all three regions contracted the fundus strip. The contractions were due to at least two substances as revealed by treatment of the strip with 2-bromolysergic acid diethylamide (BOL). The contractions that were sensitive to BOL are attributed to 5-hydroxytryptamine (5-HT) whereas the BOL resistant contractions appear to be due to an unknown hydroxy acid related to irin or the prostaglandins.3. The contractions produced by effluent collected from the third ventricle were due wholly or mainly to 5-HT, those from the inferior horn to the unknown hydroxy acid, and those from the anterior horn to both substances in varying proportions. In addition, some samples of effluent from the third ventricle seemed to contain catecholamines as well.4. The 5-HT in the effluent from the third ventricle is thought to be derived from the hypothalamus. The amounts assayed in 1 ml. effluent-the volume collected during 10 or 20 min perfusion-varied between 0.4 and 12 ng 5-HT. Output of 5-HT was initially high, then usually decreased but sometimes increased again during prolonged perfusion when temperature began to rise as anaesthesia lightened or when additional pentobarbitone sodium was given intravenously.5. When perfusion of the third ventricle was continued after death the 5-HT content in the effluent increased 3 to 24-fold during the first hour and then gradually declined. This post mortem rise in 5-HT output suggests an abnormal state of release of 5-HT from the hypothalamus. The theory is discussed that the same may happen in certain cases of brain injury and that the abnormal release of 5-HT would explain the pyrexia and shivering seen in such cases.6. The intraperitoneal injection of 5-hydroxytryptophan greatly increased the output of 5-HT in the effluent from the perfused third ventricle but only when this precursor of 5-HT was injected in large doses which caused respiratory arrest thus necessitating artificial ventilation. Upon the injection of 150 mg/kg the output of 5-HT rose to 90 ng/ml. and a further rise to 180 ng/ml. occurred when perfusion was continued after death.7. It was not possible to establish a relation between the presence of the hydroxy acid in the effluent from the inferior horn and neuronal activity.8. The 5-HT detected in the effluent from the anterior horn is assumed to have been released from the caudate nucleus.

5-Hydroxytryptophan↗
PubMed1966

Effect of 5-hydroxytryptophan acting from the cerebral ventricles on 5-hydroxytryptamine output and body temperature.

1. In cats anaesthetized with intraperitoneal pentobarbitone sodium the third ventricle, the anterior or inferior horn of the left lateral ventricle, was perfused with 5-hydroxytryptophan (5-HTP) in different concentrations, and the effluent assayed for 5-hydroxytryptamine (5-HT) on the rat stomach strip preparation of Vane (1957).2. On perfusion of the third ventricle with 5-HTP the output of 5-HT in effluent increased, the increase depending on the 5-HTP concentration: with 1/50,000 it increased 44-69 times (mean 55), with 1/25,000, 81-83 times (mean 82) and with 1/10,000, 71-200 times (mean 128). The 5-HT output depended also on the initial output during the preceding perfusion with artificial c.s.f. The greater this initial output the greater was the maximum output reached during the 5-HTP perfusion.3. The increase in 5-HT output during perfusion of the third ventricle with 5-HTP was usually associated with shivering and a rise in rectal temperature. This association, however, was not invariably obtained, probably because of a central depressant effect of 5-HTP itself.4. On perfusion of the anterior or inferior horn of the left lateral ventricle with 5-HTP, the output of 5-HT in the effluent also increased, but to a lesser extent than in the effluent from the third ventricle. There was no association with shivering nor with a rise in rectal temperature.5. An injection of 1 or 2 mg 5-HTP into the cerebral ventricles of unanaesthetized cats produced a biphasic rise in temperature, shivering, constriction of the skin vessels followed by vasodilatation, tachypnoea, wiping and scratching movements, miaowing and long lasting sleep.6. The biphasic rise in temperature is explained as the result of two opposing effects: increased formation of 5-HT which would raise body temperature, and a central depressant effect of 5-HTP itself or of one of its metabolites which would lower body temperature.7. The initial rise in temperature and the shivering in response to an intraventricular injection of 5-HTP varied from cat to cat. In those in which these effects were strong the 5-HT output during a subsequent perfusion of the third ventricle with artificial c.s.f. was higher, and the maximum 5-HT output reached on perfusion with 5-HTP was greater than in those in which these effects had been weak.

5-Hydroxytryptophan↗
PubMed1966

Effects on temperature of monoamines injected into the cerebral ventricles of anaesthetized dogs.

1. In dogs anaesthetized with pentobarbitone sodium an injection of adrenaline or noradrenaline into the cerebral ventricles through a cannula implanted into the left lateral ventricle caused a fall in rectal temperature as a result of cessation of shivering, loss of muscle tone, and skin vasodilatation. 5-Hydroxytryptamine (5-HT) similarly applied caused shivering and a rise in rectal temperature.2. The hypothalamus of the dog thus appears to react to the three monoamines in the same way as in the cat, and not as in the rabbit and sheep.

Animals↗