PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Central Nervous System Effects”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1979

Four stimulants of the central nervous system: effects on short-term memory in young versus aged monkeys.

Aged Rhesus monkeys and young control monkeys were tested in a delayed-response procedure to assess the effects of central-nervous-system (CNS) stimulants on short-term memory (STM). Previous research had established that the aged monkeys showed specific impairments of STM in this procedure. Four different CNS stimulants (methylphenidate, magnesium pemoline, a pentylenetetrazole/niacin mixture, and caffeine) were chosen for evaluation on the basis of their relevancy to current geriatric-psychopharmacologic research. Four different doses of each of the four CNS stimulants were given to each monkey, counter-balanced for possible order effects. Methylphenidate and caffeine impaired the performance of both age groups in this non-human primate cognitive task, even at relatively low dose levels. Magnesium pemoline produced fewer adverse effects and some evidence of improving STM in the aged monkeys, although not within the levels of statistical significance. The pentylenetetrazole/niacin mixture produced a three-way interaction involving age, dose and retention interval. This reflected the fact that although no definite effects were noted under the zero-sec control condition, statistically significant age-related deficits did occur in the STM-dependent retention interval as the dose varied. The data demonstrate that, of these four CNS stimulants, none radily improves (and often may impair) performance of tasks requiring STM. Thus the results of this study offer little support for the hypothesis that general CNS stimulation may constitute significant therapy for cognitive impairments associated with advanced age.

Aging↗
PubMed1977

Neurotensin: central nervous system effects of a hypothalamic peptide.

The central administration of neurotensin, an endogenous hypothalamic tridecapeptide, produces a marked dose-related decrease in body temperature of mice and rats at an ambient temperature of 25 degrees C. This effect is even more pronounced when mice are placed at 4 degrees C to increase the rate of decline of body temperature. Other sequelae observed after central administration of neurotensin are decreases in locomotor activity in rats and a marked dose-related enhancement in pentobarbital-induced mortality, sedation and hypothermia. This latter effect was shown to be due to a significant reduction in the metabolic degradation of the barbiturate. None of the above-mentioned effects are observed after peripheral neurotensin administration, suggesting that this peptide does not readily cross the blood-brain barrier. Neurotensin appears to be one of a growing list of neuropeptides that can affect CNS function.

Animals↗
PubMed1977

Dopamine receptor blocking activity of sulpiride in the central nervous system.

Effects of sulpiride on the central nervous system were studied in catalepsy induction (I) and antagonism to gnawing behaviour (II) induced by apomorphine and methamphetamine in normal rats, and in antagonism to rotational behaviour (III) induced by apomorphine and methamphetamine in rats with substantia nigra unilaterally lesioned chronically by microinjection of 6-hydroxydopamine. Sulpiride was administered orally and intraventricularly, and the effects of sulpiride were compared to those of haloperidol and chlorpromazine administered through the same routes. In oral administration, sulpiride was almost inactive in (I), and was several hundreds to a thousand times less potent than haloperidol in (II) and (III), while chlorpromazine was 20 to 150 times stronger than sulpiride. In intraventricular administration, sulpiride was almost equipotent to haloperidol in (I), and was equally effective to or 2 to 3 times more effective than halopridol in (III), although several times less in all respects. These findings suggest that sulpiride is essentially a potent inhibitory substance on dopamine receptors in the central nervous system and the rather weak central effects of peripherally given sulpiride are due to poor penetration through the blood brain barrier.

Administration, Oral↗
PubMed1975

Central nervous system effects of local anaesthetic agents.

A review is given of an experimental study on cats where the influence of acid-base changes on central nervous system toxicity of local anaesthetic agents was studied. The conclusion of this study was that a respiratory acidosis increased the central nervous system toxicity of local anaesthetics and that the underlying metabolic conditions modified this increase. Thus a respiratory acidosis increased this toxicity more if it was based on a metabolic acidosis than on a metabolic alkalosis (Englesson, 1974; Englesson and Grevsten, 1974). An extended analysis is presented where automatic frequency analysis was performed on the e.e.g. recordings performed during the i.v. infusion of lignocaine, bupivacaine, L 134, HS 37 and its optical isomers. The preliminary results show that the electrical changes appearing in the e.e.g. from the start of the i.v. infusion until seizure activity were the same if this time interval was as short as 1 min or as long as 8 min. It also revealed remarkable individual differences between agents, for instance lignocaine displaying marked electrical changes already in the first third of this time period where bupivacaine showed no changes until shortly before seizures.

Acid-Base Equilibrium↗
PubMed1979

Cardiovascular and subjective central nervous system effects of long-acting local anaesthetics in man.

Intravenous infusions of etiodocaine 50, 75 and 100 mg and bupivacaine 75 mg were carried out over ten minutes in healthy young adult males. Cardiovascular sequelae were generally trivial at all doses. A collection of subjective central nervous system symptoms were described which may be regarded as early warning of impending local anaesthetic toxicity. Plasma concentrations of etidocaine were proportional to dose and ranged from 2 micrograms/ml to 5 micrograms/ml at the termination of the infusion. Plasma concentrations of bupivacaine were similar to those from the same dose of etidocaine but declined more slowly on cessation of infusion.

Acetanilides↗
PubMed1975

Central nervous system effects of hypothalamic peptides.

Intravenous (i.v.) administration of TRF (1 mg/kg) increases the LD50 of pentobarbital (PB) by 25% while the same dose of somatostatin results in a 30% reduction in PB LD50. A similar increase of PB LD50 by TRF was observed in hypophysectomized rats. Mortality was completely abolished in rats receiving TRF (1 mg/kg) ten minutes after a lethal dose of PB (120 mg/kg). Somatostatin (1 mg/kg) decreases strychnine-induced seizure duration and increases strychnine LD50 by 21% while TRF lowers the strychnine LD50 by 28%. These observations are consistent with central nervous system sites of action for TRF and somatostatin.

Animals↗
PubMed1979

Synthesis of some carbon-3 substituted 1,4-benzodiazepin-2-ones and their central nervous system effects.

Starting from 3-hydroxy-1,4-benzodiazepin-2-ones 1--3, via 3-chloro derivatives 4--6, 13 new C(3)-substituted 1,4-benzodiazepin-2-ones were synthesized. Reaction of 4--6 with ethylene glycol yielded 3-(beta-hydroxyethyl) derivatives 7--9. Similar reaction with the isopropylidene derivative of glycerol afforded 10--12, which on hydrolysis of the isopropylidene group hielded glycerol derivatives 13--15. Reaction of trichloroacetyl chloride with oxazepam and temazepam yielded the corresponding trichloroacetyl esters 16 and 17. The beta-hydroxyethyl derivative 7 was conjugated with an acetylated glucopyranose derivative to give isomeric 18 and 19. Partition coefficients (log Poct) and central nervous system activities (in six stranded tests) were determined for 7--15 as well as several standard compounds. Most of the compounds exhibiting beneficial central nervous system activity had Poct values between 1.71 and 2.48. No correlation between lipophilicity and central nervous system activity could be discerned for these compounds.

Animals↗
PubMed1977

Interaction of central nervous system effects of high pressures with barbiturates.

The interactions of phenobarbital, barbital, and pentobarbital with high pressures of heliox were explored. Principal features of the complex results include: double peaks in the time course of convulsion thresholds (Pc); an early peak and a shoulder in the time course of pressures reversing anesthesia (Pa); far steeper dose-response curves for Pa than for Pc; selectively greater anticonvulsant effect for phenobarbital than for the other barbiturates; and enhancement of Pa with simultaneous depression of Pc by reserpine in phenobarbital-pretreated mice. The data indicate the existence of at least two discrete sites of interaction between barbiturates and high pressure, reflected by Pc and Pa. The implications of the data for the development of biophysical theories of pressure reversal of anesthesia and anti-high-pressure neurological syndrome action of anesthetics are discussed, together with implications for the experimental study of convulsant and anticonvulsant agents, and their applications to underwater physiology.

Animals↗
PubMed1976

Relation between drug-induced central nervous system effects and plasma levels of diazepam in man.

Pharmacodynamic effects and plasma levels of diazepam were studied in healthy male volunteers at different dose levels. Responses to diazepam were quantified, using instruments which measured body sway (statometry) and psychomotor performance (stressalyser tests). High dose-related correlations were obtained between drug-induced changes in test parameters and drug plasma levels, both with regard to stimulant and depressive effects. Techniques were devised for evaluating and comparing the efficacy and usefulness of different types of tests, taking into account critical thresholds, slopes and error estimates, correcting for changes in predrug levels and control (nondrug) trials.

Adolescent↗
PubMed1976

[Pharmacodynamics of 2-(4-benzyl-piperidino)-1-(4-hydroxyphenyl)-1-propanol (Ifenprodil). (3) Effects on the autonomic, peripheral and central nervous systems].

Effects of ifenprodil tartrate, a potent vasodilator, on the autonomic, peripheral and central nerve system were studied in experimental animals. In isolated vas deferens of guinea pigs, the contraction in response to noradrenaline and sympathetic nerve stimulation was competetively antagonized by ifenprodil 10(-7)--10(-5) M (pA2: 7.69 against noradrenaline). Ifenprodil (50 approximately 1,000 mug/kg i.v.) inhibited the contraction of cat nictitating membrane and dog urinary bladder induced by sympathetic nerve stimulation. Ifenprodil (250 approximately 1,000 mug/kg i.v.) lowered adrenaline-induced lethality (ED50: 360 mug/kg). The drug produced a hypermotility of guinea pig uterus, and showed a transient hypertonus of dog gut which was abolished by atropine. Ifenprodil (10 approximately 20 mg/kg i.v.) inhibited the propulsion of charcoal meal in mice. In Shay rats, more than 10 mg/kg i.m. of the drug inhibited the secretion of acid gastric juice and the ulceration. Ifenprodil showed a potent local anesthetic action in the guinea pig cornea and skin. The spontaneous EEG of rabbits showed a resting pattern (0.25 approximately 2 mg/kg i.v.) followed by an arousal pattern (5 approximately 10 mg/kg). Ifenprodil (20 approximately 100 mg/kg p.o.) potentiated a hypnosis induced by barbital, and potentiated pentylenetetrazol, strychnine and picrotoxin induced convulsion. The drug (20 and 100 mg/kg p.o.) lowered the body temperature of rats. From these results it is concluded that ifenprodil produces a blocking action of alpha-adrenoceptors in various smooth muscle preparations and a direct relaxation of the smooth muscle itself without affecting the motor and central nerve systems.

Animals↗
PubMed1978

Saralasin and SQ 20881 : their effects on central nervous system norepinephrine.

The effects of the infusion of Saralasin and SQ 20881, two drugs that inhibit the renin-angiotensin system, on the norepinephrine (NE) concentration in hypothalamus and medulla oblongata were studied in male Wistar rats. NE content increased in hypothalamus in response to both drugs, without changes in medulla oblongata catecholamine concentration. These results showed that the NE concentration of certain areas of the central nervous system can be modified, in a short time, by the inhibition of the renin-angiotensin system. Results observed after the infusion of Saralasin could indicate that the receptors, on which the angiotensin acts to produce this alteration, are similar to those of the peripheral blood vessels.

Angiotensin II↗
PubMed1978

Effects of intraventricular angiotensin II mediated by the sympathetic nervous system.

Central effects of angiotensin II were studied in rats treated with adrenalectomy, chemical sympathectomy with intravenous 6-hydroxydopamine, or a combination of both. Unrestrained, unanesthetized rats were compared before and after one of the three treatments to determine water drinking and blood pressure responses to intracerebroventricular (ivt) injections of 50 and 500 ng angiotensin II (AII). Adrenalectomy alone did not alter either drinking or pressor response to AIIivt. Peripheral sympathectomy alone resulted in a prolonged latency for pressor response but did not significantly alter drinking response to AIIivt. Results obtained by combined treatment were not significantly different from results obtained by sympathectomy alone. There remained a pressor response to AIIivt after combined treatment. The adrenals do not appear to be involved in mediating pressor response to AIIivt. Furthermore, sympathetic neural activation alone causes the early pressor response to AIIivt. Finally, some other factor(s) in addition to sympathetic neural activation must contribute to the pressor response to AIIivt.

Adrenalectomy↗