Effects of the intracerebroventricular administration of ketamine on centrogenic arrhythmias in anesthetized rats.

In urethane anesthetized rats the icv (lateral cerebral ventricle) administration of ketamine, at the highest utilized doses, induced bradypnea and sinus bradycardia in spontaneously breathing rats. Moreover, it partially antagonized the arrhythmogenic activities of sodium glutamate and sodium aspartate, as well as desipramine and ouabain. From these results, we conclude that ketamine had an inhibitory effect on the centrogenic arrhythmias not only acting at the level of NMDA subtype receptor, but also at beta 1 adrenergic central receptors. Moreover at high doses, ketamine can also induce centrogenic arrhythmias in spontaneously breathing rats.

Central antiarrhythmic effects of imidazole in anesthetized rats.

In urethane anesthetized rats, the intracerebroventricular (icv.) microinjection of sodium glutamate or KCl induced cardiac arrhythmias. These cardiac rhythm disorders could be prevented by the icv. administration of imidazole. The i.v. injection of the same doses of imidazole elicited cardiac arrhythmias. The antiarrhythmic activity of imidazole is probably due to its ability to stimulate phosphodiesterase activity, which leads to a decrease in cGMP and/or cAMP cerebral levels.

The effect of some enkephalins on calcitonin secretion.

Synthetic enkephalins: 5 metenkephalin, D2 proenkephalin and 5 leuenkephalin and morphine were injected into cerebral ventricles of rats. After 30 minutes the rats were sacrificed and the calcitonin content of the thyroid was assayed. As compared to the controls, morphine reduced significantly the secretion of calcitonin. Of the enkephalins, only 5 leuenkephalin had a borderline effect on calcitonin secretion, stimulating to a significant degree the rise of the hormone. The data obtained demonstrate the selective effect of opiates on calcitonin secretion.

Interactions of propranolol with some analgesics.

The duration of the analgesic effect of levomepromazine was prolonged in mice when associated with propranolol. The administration of morphine to animals treated with propranolol resulted in an increase of morphine toxicity with death of some animals.

Cardiovascular effects of amphepramone.

The i.v. administration of amphepramone in dogs induced a dose-related depressor reaction. This effect was due to a peripheral myotropic vasodilatation. When the drug was administered intracerebroventricularly it elicited a marked pressor response, due, to the release of catecholamines with its subsequent action on alpha-adrenergic receptors. Small doses of amphepramone administered in dogs, rats and rabbits, induced a sinus tachycardia. Larger doses brought about a sinus bradycardia, bradyarrhythmias, extrasystoles, ventricular bradycardia and ventricular fibrillation or asystolia. The respiratory movements as well as the EEG tracings were depressed by larger doses of amphepramone.

Some central nervous actions of centrophenoxine (Meclofenoxat) in animals.

In experiments with rats and mice it was been found that centrophenoxine in acute experiments in large doses has inhibitory effects on the central nervous system. Centrophenoxine has no analgesic action. When administered subchronically, centrophenoxine aggravates both the pentetrazol and the maximal electroshock seizures.

Reflex and neuro-humoral pressor action of the hypertonic solutions.

The intraarterial injections of 50% urea or 20% NaCl induced a rise of the systemic arterial blood pressure simultaneously with a constriction of the vessels of the legs. The mechanism which is responsible for these phenomena is very complex. It includes a reflex arising from the arterial wall, which is mediated through the spinal cord, the release of catecholamines and of some still nonidentified pressor substances and a central component which is normally masked by the depressor sinus reflex.

Experimental observations on the effect of amphepramone on the behavior, locomotion, pentretrazol seizures and electroencephalogram.

Amphepramone, an anorectic agent, has been found to possess stimulant properties on the C.N.S. in animals, producing hypermotility and stereotyped movements which can be antagonized with neuroleptics. The stimulant activity of amphepramone observed in animals can be correlated with the amphetamine like psychosis observed in humans.

Some behavioural changes induced by amantadine (adamantine).

In experiments carried out in mice, it was shown that amantadine (adamantine) (50, 75, 100 and 200 mg/kg i.p.) reduced the exploratory activity. This phenomenon was due not to reduction of the locomotion and of the muscular force. Amantadine in large doses had a slight convulsant action; at the same dose (100 mg/kg i.p.) it greatly potentiated the convulsant effects of pentetrazol. On Haffner's test amantadine had no analgesic activity.