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Biomedical subjects

R Samardzić

Publications and source records attributed to R Samardzić.

At least 37 records · Page 2Linked to original sources
PubMed1986

Comparative behavioral effects of anticholinergic agents in cats: psychomotor stimulation and aggression.

The effect on behavior of eight anticholinergic agents: atropine, scopolamine, trihexyphenidyl, biperiden, homatropine, eucatropine, hexocyclium and propantheline, injected into the cerebral ventricle (ICV) of the cat was investigated and compared. The anticholinergic agents evoked: (1) psychomotor stimulation such as miaowing, loud calling, restlessness, impelling locomotion, jumping, vacant staring, apprehension and loss of interest of the surroundings; (2) aggression, hissing, threat, attack, defense, fighting with paws and flight; (3) autonomic responses including mydriasis, tachypnea, dyspnea, licking, vomiting, salivation, micturition and defection; and (4) motor phenomena comprising scratching, ataxia, rigidity, tremor, weakness with adynamia or myoclonic jerks. Convulsions appeared only after ICV injections of atropine and homatropine. The most characteristic behavioral effect of anticholinergic agents was psychomotor stimulation accompanied by mild aggressive responses. The only exception was propantheline which caused a muscular weakness and adynamia. Atropine and scopolamine alone induced a dose-dependent impelling locomotion as well as fighting behavior. Carbachol and eserine injected intracerebroventricularly reversed the locomotion autonomic and motor phenomena produced by anticholinergic agents administered similarly. It is suggested that anticholinergic agents acting as partial agonists, can produce their behavioral effects through central cholinoceptive sites.

Aggression↗
PubMed1985

Behavioral, autonomic and motor effects of neuroleptic drugs in cats: motor impairment and aggression.

The effects of eight neuroleptic drugs injected into the cerebral ventricles on behavior, autonomic and motor activity of unanesthetized cats have been studied. Chlorpromazine, trifluorpromazine, droperidol, haloperidol, domperidone and spiperone induced emotional behavior (restlessness, miaowing, rage, attack, defense, fighting with paws, biting), autonomic (mydriasis, tachypnoea, dyspnoea, panting, salivation, defecation, urination, licking, vomiting) and motor (ataxia, muscular weakness, adynamia) phenomena. The main and the most consistent effect was the motor impairment, while the aggression was inconsistent and of moderate intensity. Of the neuroleptic drugs injected, only spiperone, domperidone and trifluorpromazine produced a dose-dependent motor impairment. The autonomic effects were also inconsistent and of low intensity. Metoclopramide induced inconsistent autonomic and motor effects, while sulpiride was devoid of any visible behavioral, autonomic and motor activity. It appears, therefore, that the motor impairment as well as the aggression caused by the neuroleptic drugs is perhaps related to central D-1 rather than to central D-2 dopamine receptors, but an effect on central norepinephrine and on central serotonin receptors cannot be excluded.

Aggression↗
PubMed1985

The effect of nifedipine and verapamil on the pendular movements of the rabbit isolated ileum.

The inhibitory effect of calcium antagonists such as nifedipine and verapamil on the pendular movements of the rabbit isolated ileum was investigated. Nifedipine and verapamil depressed or abolished the pendular movements. The inhibitory effects of nifedipine and verapamil were concentration-dependent. Nifedipine is about 1000 times more potent than verapamil. Calcium ions failed to reverse the inhibitory effects of nifedipine and verapamil. Calcium antagonists which influence the motor activity of the digestive tract, therefore, could have therapeutic use independent of their action on the cardiovascular system.

Animals↗
PubMed1984

[Psychomotor excitation caused by beta-endorphin: effect of rubidium and lithium].

Effects of lithium and rubidium administered into the cerebral ventricles of conscious cats on psychomotor excitation produced by synthetic human beta-endorphin similarly injected have been investigated. Lithium, but not rubidium, prevented the psychomotor stimulation caused by beta-endorphin. Naloxone, applied intracerebroventricularly, also prevented the psychomotor stimulation produced by this polypeptide. It appears, therefore, that only lithium has a psychotherapeutic value when homeostatic neurohumoral mechanisms are disturbed in the central nervous system by a surplus of beta-endorphin.

Akathisia, Drug-Induced↗
PubMed1984

[Differences in the action of enkephalins, beta-endorphin, and morphine on spontaneous rhythmic movements of the isolated rabbit ileum].

Methionine-, leucine-enkephalin and beta-endorphin produced dose-related depression followed, not regularly, by stimulation of the spontaneous rhythmic activity of rabbit isolated ileum. The stimulant effect was obtained in one third to one half of the experiments. Naloxone antagonized the depressant, but not the stimulant effects of enkephalins and beta-endorphin. Morphine depressed or stimulated the spontaneous rhythmic activity of rabbit isolated ileum, but only when this narcotic analgesic was used in extremely large amounts. Naloxone had no effect or potentiated the depressant effect, while it potentiated the stimulant effect of morphine. It is apparent, therefore, that only enkephalins and beta-endorphin depressed the spontaneous rhythmic activity of rabbit isolated ileum by acting on enkephalinergic receptors. Further, these results suggest that these enkephalinergic receptors may be involved in the modulation or transmission of spontaneous rhythmic activity of rabbit isolated ileum.

Animals↗
PubMed1984

[Effects of nifedipine and verapamil on body temperature in cats].

Nifedipine and verapamil injected into the cerebral ventricles of unanaesthetized cats produced a longlasting rise in the body temperature. The hyperthermic effect of nifedipine and verapamil were not dose-dependent. The hyperthermic effect of verapamil was preceded by a shortlasting fall in the body temperature, which was not dose-dependent. Calcium antagonists, nifedipine and verapamil also produced mydriasis, tachypnoea, dyspnoea, ataxia, tremor and muscular weakness. These symptoms were inconsistent and of slight intensity. In agreement with the theory of ionic set point controlling the body temperature, the most probable explanation is that calcium antagonists, nifedipine and verapamil produced changes in the body temperature by acting on sodium and calcium fluxes in the posterior hypothalamus.

Animals↗
PubMed1982

Differences in central effects of beta-endorphin and enkephalins: beta-endorphin. A potent psychomotor stimulant.

The endogenous opiate-like peptides, beta-endorphin, methionine- and leucine-enkephalin have been investigated in unanaesthetized cats after intracerebroventricular injection. beta-Endorphin produced marked and prolonged psychomotor stimulation (restlessness, apprehension, looking around, vacant stare and impelling locomotion), accompanied by pupillary dilation and tremor which was prevented by nalorphine. In contrast to beta-endorphin, the enkephalins did not cause affective behavioural phenomena. However, the enkephalins evoked transient and inconsistent vomiting which was also prevented by nalorphine. It is apparent, therefore, that morphinomimetic brain peptides are involved in at least two functions in the central nervous system: beta-endorphin subserves the mediation of a long-lasting psychomotor stimulation, while the enkephalins mediate vomiting of a transient character.

Akathisia, Drug-Induced↗
PubMed1982

beta-Endorphin-induced psychomotor excitation in the cat.

The effect on behavior of synthetic human beta-Endorphin injected into the cerebral ventricles of the cat was investigated in these experiments. beta-endorphin produced psychomotor excitation (i.e., restlessness, apprehension, flight and locomotion), accompanied by pupillary dilatation and tremor. Between periods of locomotion, the cat sat moving its head from side to side with eyes wide open and mydriasis, or stood stiffly with a vacant stare, pupils dilated and eyes wide open. During this time the cat did not react to objects moving in front of it. Behavioral changes produced by a single dose of beta-endorphin were dose-dependent and long-lasting. Pretreatment with intracerebroventricular nalorphine depressed or abolished the behavioral changes, mydriasis and tremor caused by beta-endorphin. It is concluded that beta-endorphin acts on central opiate receptors promoting psychomotor excitation.

Animals↗
PubMed1982

Inhibition by lithium of beta-endorphin-induced psychomotor excitation in cats.

beta-Endorphin injected into the cerebral ventricles of unanesthetized cats produced dose-dependent and long-lasting restlessness, locomotion, stereotyped sideways movements of the head, vacant staring, apprehension and flight accompanied with mydriasis and tremor. The most impressive features of the psychomotor excitation were the locomotion and the sideways movements of the head. Intracerebroventricular nalorphine prevented the psychomotor excitation caused by intracerebroventricular beta-endorphin. Lithium chloride and lithium carbonate injected into the cerebral ventricles prevented and reversed the psychomotor excitation evoked by beta-endorphin similarly injected. In cats showing spontaneous locomotor activity, intracerebroventricular lithium chloride also suppressed this activity. It is suggested that beta-endorphin elicited psychomotor excitation by acting on central opiate receptors. However, the effect of lithium cannot be solely ascribed to an action on central opiate receptors and endogenous peptides. Since lithium affected the spontaneous as well as the beta-endorphin-induced locomotion, it may be supposed that the cation suppressed the ongoing input activity at central locomotion activity levels.

Animals↗
PubMed1982

[Inhibitory effect of magnesium on the vocalization and fighting of cats treated with carbachol and eserine].

Magnesium sulfate injected into the cerebral ventricles of conscious cats inhibited the vocalization and the fighting evoked by intracerebroventricular injections of carbachol and eserine. The magnesium completely blocked the convulsions caused by eserine, but had no effect on the convulsions produced by carbachol. Other motor phenomena and signs of autonomic activation produced these cholinergic agents were not significantly altered by MgSO4.

Aggression↗
PubMed1982

[Effect of nicergoline and dihydroergotamine, injected into the cerebral ventricles, on arterial pressure in the cat].

Nicergoline, injected into the cerebral ventricles of anaesthetized cats induced a moderate, but longlasting and dose-dependent fall of the blood pressure. Dihydroergotamine, in moderate doses, had no effect on the arterial blood pressure. Toxic doses of nicergoline and dihydroergotamine provoked a pronounced fall of the arterial blood pressure and inhibition of the respiration. Bradycardia only appeared after toxic doses of dihydroergotamine. It is concluded that the hypotensive effect of nicergoline is at least in part central in origin.

Animals↗
PubMed1981

6-hydroxydopamine and aggression in cats.

The effect of 6-hydroxydopamine (6-OHDA) injected into the cerebral ventricles on behaviour of singly- and group-housed cats was investigated. 6-OHDA in doses of 0.5, 1 and 2 mg was administered every morning for 5 to 8 days. In small doses 6-OHDA in singly- and group-housed cats evoked motor phenomena such as tremor, ataxia, rigidity, weakness and sometimes clonic-tonic convulsions. Occasionally restlessness, irritability and rage were observed. Large doses of 6-OHDA in group-housed cats, after a short latent period (2-3 days) produced aggression which intensified on subsequent injections, and thereafter, on repeated administrations, no longer occurred. The aggression consisted of restlessness, irritability, anger, rage, apprehension, threat, attack, fighting, flight and crying. Of autonomic phenomena mydriasis, dyspnea and sometimes piloerection were observed. The aggression was initiated by the most restless cat, or by disturbing the animals, such as by moving the cage. When 6-OHDA no longer produced aggressive behaviour, motor changes such as tremor, ataxia, rigidity, walking on broad base, weakness with adynamia and clonic-tonic convulsions developed. These latter symptoms were produced by large doses of 6-OHDA in singly-housed cats. In these animals spontaneous signs of aggressive behaviour usually were not observed, although if handled they showed rage, snarling and hissing. When singly-housed cats were kept in the same cage with group-housed animals, the singly-housed cats usually became aggressive. It appears that hyperactivity induced aggression in 6-OHDA-treated cats.

Aggression↗