Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Apomorphine”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 865 records · Page 48Linked to original sources
PubMed2004

Literature review: intermittent subcutaneous apomorphine therapy in Parkinson's disease.

Apomorphine injectable has been used in Europe for more than a decade as a rescue therapy for intractable "off" periods in Parkinson's disease (PD). Some studies were performed as early as the 1970's. This article reviews double-blind and open studies with apomorphine for PD prior to the year 2000. Most were performed in Europe. Double-blind studies with injection doses of 1-5 mg have demonstrated that onset of clinical benefit typically occurs within 10 minutes, and lasts for up to two hours. The magnitude of benefit rivals that of levodopa. Long-term, open-label studies have demonstrated the persistent response to apomorphine injectable as a rescue therapy for as long as five years. Duration of benefit and dose of a single injection remains the same, but a need for increased number of doses per day is reported in keeping with disease progression. For many patients, the need for concomitant domperidone administration for antiemesis wanes over time. Apomorphine has also been shown in smaller studies to be effective for a variety of non-motor "off" phenomena, including pain, panic attacks, and a variety of gastrointestinal symptoms. Subutaneous intermittent bolus injects are also useful in patients post operatively who are unable to take oral medications.

Antiparkinson Agents↗
PubMed1998

Further evidence for interaction between angiotensin II and dopamine receptors (experiments on apomorphine stereotypy).

The present study was undertaken to further evaluate the effects of angiotensinergic agents: angiotensin II (AII), its analogues sarmesin ([Sar1, Tyr(Me)4]AII) and sarilesin ([Sar1, Ile8]AII), as well as DuP 753, a nonpeptide selective AT1 receptor antagonist, on apomorphine stereotypy in rats thus providing further evidence for AII-DAergic receptor interactions. All drugs were administered intracerebroventricularly (i.c.v.). Stereotyped behavior was evoked by an i.p. injection of 3 mg/kg apomorphine. AII (0.1-5 micrograms) exerted a decrease on stereotypies (U-shaped); the effect being significant at doses of 1 and 2 micrograms. Sarmesin significantly increased apomorphine stereotypy at a dose of 5 micrograms and decreased it at a dose of 20 micrograms. Sarmesin (10 micrograms) reversed the decreasing effect of AII (2 micrograms) leading to a more pronounced increase of stereotypies. Sarilesin (5 micrograms), which by itself is inactive, also demonstrated antagonistic properties when injected 5 min before AII (2 micrograms). DuP 753 (100 micrograms) alone had no significant effect on apomorphine stereotypy, but injected 5 min before AII (2 micrograms) it reversed the decreasing effect of AII on stereotypy. Taken together, the results further confirm the hypothesis that AII closely interacts with DAergic neurotransmission, an effect which is mediated predominantly by AT1 receptors.

Angiotensin II↗
PubMed1991

Hormonal effects of apomorphine and cholecystokinin in pigs: modification of the response to cholecystokinin by a dopamine antagonist (metoclopramide) and a kappa opioid agonist (PD117302).

Three experiments were carried out to investigate some of the mechanisms involved in the endocrine responses of pigs to the emetic agents apomorphine and cholecystokinin. In Experiment 1, plasma levels of vasopressin and cortisol were measured in prepubertal pigs (N = 5) treated with i.v. apomorphine (25 micrograms/kg) or saline vehicle. In Experiment 2, concentrations of vasopressin and cortisol were determined in pigs given iv sulphated cholecystokinin octapeptide (1.3 micrograms/kg), metoclopramide (300 micrograms/kg), metoclopramide + cholecystokinin, and an oral dose of the kappa opioid agonist PD 117302 (20 micrograms) alone, or followed by i.v. cholecystokinin. In Experiment 3, operant feeding behaviour was quantified in pigs (N = 4) given cholecystokinin (1 microgram/kg) or cholecystokinin preceded by oral PD 117302. Following apomorphine injection in Experiment 1, there was a rapid, transient, rise in plasma vasopressin. Cholecystokinin had a similar effect on vasopressin secretion in Experiment 2 and also induced a later rise in plasma cortisol. Pre-treatment with metoclopramide appeared to reduce both of these effects of cholecystokinin, but only the decrease in cortisol was statistically significant. However, oral administration of PD 117302 abolished the effect of cholecystokinin on vasopressin release and reduced the subsequent rise in cortisol. The inhibitory effect of cholecystokinin on feeding was unaltered by PD 117302 treatment in Experiment 3. The results obtained with apomorphine and metoclopramide, together, suggest that the neuroendocrine effects of cholecystokinin in the pig may involve an action on central dopamine receptors while the effects of PD 117302 indicate that kappa opioids may modify the hormonal responses to cholecystokinin by a peripheral action.

Animals↗
PubMed1975

Effect of apomorphine on the canine SA node.

A constant pressure perfusion of the sinus node artery was performed in 10 in situ and in 3 isolated SA node preparations. The selective administration of apomorphine caused a negative chronotropic effect which was not blocked by treatment with atropine. The sinus deceleration was usually produced by apomorphine, 10-300 mug, while sinus irregularity and finally atrioventricular nodal rhythm in the in situ preparation or sinus arrest in the isolated one resulted from doses above 1 mg. In the in situ preparation at a higher dose from 300 mug to 1 mg, a slight sinus acceleration was occasionally induced following sinus deceleration; In this time, a fall in blood pressure was usually observed; This acceleration response to apomorphine was inhibited by propranolol. From these results, it is concluded that apomorphine induces direct depressive action on the SA node and, in extremely high doses, a slight sinus acceleration may be induced by reflex mechanism.

Animals↗
PubMed1975

The influence of 2 br-alpha-ergocryptine (CB-154) and apomorphine on induced prolactin secretion in the crab eating monkey (Macaca fascicularis).

The influence of apomorphine and 2 Br-alpha-ergocryptine (CB-154) on drug-induced prolactin secretion was examined in an intact and an ovariectomized monkey (Macaca fascicularis). Perphenazine administered iv at one mg/kg BW induced a rapid and marked increase in serum prolactin. Apomorphine at a concentration of 4 mg/kg BW administered prior to perphenazine delayed the perphenazine-induced prolactin rise. The iv administration of CB-154 at either 200 or 2000 mu-g/kg BW completely blocked the perphenazine response. Apomorphine injected before TRH suppressed the induced prolactin increase to this releasing hormone while CB-154, even at the very high dose, only partially blocked the TRH-induced prolactin rise. Serotonin injected iv at the level of 10 mg/kg BW induced a rapid and marked increase in serum prolactin and both apomorphine and CB-154 were able to block this response.

Animals↗
PubMed1975

Thyrotropin-releasing hormone blockade of the ergocryptine and apomorphine inhibition of prolactin release in vitro.

The interaction of thyrotropin-releasing hormone (TRH) and ergocryptine or apomorphine in affecting prolactin secretion was examined. Ergocryptine and apomorphine inhibited the release of 3H-prolactin labeled in an in vitro incubation of the rat anterior pituitary and led to a retention within the gland of 3H-prolactin. TRH (1.4 X 10(-8) M) partially blocked the inhibitory effect of 4 x 10(10) M ergocryptine on 3H-prolactin release and totally blocked the effect on radioimmunoassayable prolactin release. TRH also completely blocked the inhibitory effects of 5 x 10(-8) M apomorphine on both 3H-prolactin and radioimmunoassayable prolactin release. Since TRH can also completely block the inhibitory effects of dopamine upon prolactin secretion, these results are consistent with apomorphine and ergocryptine stimulating "dopaminergic" sites and also further support the role of TRH as a prolactin-releasing factor.

Animals↗
PubMed1976

The effect of apomorphine and haloperidol on the RNA content of brain structures of the rat.

At a dose of 0.5 mg/kg, apomorphine caused an increase of the RNA content of the septal nucleus of rats (n. medialis + n. lateralis + n. accumbens); after 2.5 mg/kg this effect became more marked and, in addition, there was an increase of RNA in the caudate nucleus. All effects were antagonized by 0.5 mg/kg of haloperidol. These data suggest that apomorphine acts, at different dose levels, on different sites of the brain. This might be related to the also different behavioral effects of apomorphine at those two dose levels. Haloperidol on its own caused a fall of RNA in the amygdaloid nucleus which was not counteracted by any of the two doses of apomorphine. Neither drug had any influence on hypothalamic RNA concentration.

Amygdala↗
PubMed1975

Effect of amphetamine and apomorphine on brain monoamines and behaviour in the immature and young adult rat.

In the immature rat (12-day old), amphetamine (10 mg/kg i.p.) caused an initial increase in forward locomotion, followed 15 min later by intermittent stereotyped behaviour (SB). Fifty to 65 min after injection the animals entered a phase of sleep which lasted 1-3 hrs; after this period continuous SB emerged, lasting 2-3 hrs. Brain amphetamine levels (half-life = 150 min) were elevated throughout the sequence of behavioural effects. Peak amphetamine levels were lower in the immature rat than in the adult rat. In the immature animal amphetamine caused a decrease in brain dopamine (DA) 4 hrs after injection and a sustained decrease in noradrenaline (NA) which was evident at 90 min and persisted throughout the study; a significant increase in serotonin (5HT) was evident at 15 min but had returned to normal at 90 mins. In the young adult rat (5-6 wks old), amphetamine caused an increase in forward locomotion, followed in 10-15 min by continuous SB lasting 4-4.5 hrs. The half-life of brain amphetamine was 66 min. Amphetamine increased brain DA and NA within 15 min of injection. At 90 min 5HT was elevated, DA had returned to normal but NA was still increased; thereafter the concentration of NA declined to significantly lower levels than controls and 5HT returned to normal. In the immature rat, apomorphine (10 mg/kg i.p.) caused an initial increase in locomotion which was followed 10 min later by transient intermittent SB. Following this, the animals entered a phase of sleep which lasted about 40 min before intermittent SB reemerged; this persisted for 1-2 hrs. Apomorphine caused an increase in NA and a corresponding decrease in DA at 15 and 30 mins after injection after which the levels of these amines returned to normal; 5HT levels were unchanged. In the adult rat SB commenced immediately after injection of apomorphine and lasted 70 min. There were no changes in levels of brain monoamines. There was no clear correlation between behavioural observations and levels of brain monoamines after amphetamine or apomorphine.

Animals↗
PubMedDate not supplied

[Analysis of apomorphine aggessiveness and stereotypy: role of serotonin- and cholinergic systems of the brain].

In male albino rats the electrolytic lesions of the dorsal and median raphe nuclei of the mesencephalon diminished apomorphine-induced aggressiveness (number of attacks, aggressive posture latencies) but didn't influence significantly the intensity of the stereotypy. Both the blockator of tryptophane hydroxylase parachlorophenylamine (PCPA) and 1-tryptophane did not exert any influence on behavioral effects of apomorphine. The raphe-lesion as well as PCPA decreased the level of serotonin and 5-hydroxyindoleacetic acid in the rat forebrain. PCPA decreased in raphe-lesioned rats the dopamine level too. M-cholinoblocking agent atrophine enhanced apomorphine-induced aggressiveness and stereotypy. The blockator of cholinesterase physostigmine had opposite effects. The results suggest that apomorphine induced aggressiveness depends on serotoninergic and cholinergic activity in the brain and there exists a functional link between these neuromediator systems in the CNS.

Acetylcholine↗
PubMed2003

Intravenous versus subcutaneous injections of apomorphine in rabbits: a pharmacokinetic paradox.

The objective of this investigation was an attempt to conclusively prove the accidental observation that the AUC of apomorphine in rabbits was repeatedly lower after intravenous injection compared to subcutaneous injection. Apomorphine was administered to rabbits by intravenous and subcutaneous routes at 2 different doses (0.31 mg/kg, n=10; and 0.25 mg/kg, n=6). Plasma drug concentrations were measured by HPLC-ECD and pharmacokinetic parameters were estimated by compartmental and non-compartmental approaches. The AUC of apomorphine in rabbits were: for subcutaneous injection, 14138 +/- 502 ng/ml/min and 12680 +/- 855 ng/ml/min, n=10 and 6, respectively; for intravenous injection, 11850 +/- 718 ng/ml/min and 9147 +/- 671 ng/ml/min, n=10 and 6, respectively. These AUC values were statistically significantly lower when given as intravenous injection compared to subcutaneous injection (p=0.0011 and 0.0117, n=10 and 6, respectively). The T1/2,elim values were: for subcutaneous injection, 17.1 +/- 1.70 min and 18.7 +/- 1.68 min, n=10 and 6, respectively; for intravenous injection, 15.3 +/- 1.20 min and 15.0 +/- 2.24 min, n=10 and 6, respectively. There were no significant differences between the T1/2,elim from both administration routes (p=0.3984 and 0.2158, n=10 and 6, respectively). Given the reproducibility of the results, it was concluded that the AUC of apomorphine after intravenous injection in rabbits is anomalously lower than that of subcutaneous injection.

Animals↗
PubMed1992

[Nasolabial allergic reaction to intranasal administration of apomorphine in Parkinson disease].

A patient is presented who used apomorphine, a potent dopamine agonist in the treatment of Parkinson patients. He suffered of severe dystonia of the legs, which did not respond to conservative treatment. The apomorphine was delivered bij intranasal spray. The patient developed an allergic reaction with swollen nose and lips, which disappeared within one day after discontinuation of the treatment. Subcutaneous administration caused no symptoms. Cutaneous challenge with apomorphine caused a positive reaction. We raise the hypothesis that the allergic reaction was due to the binding of apomorphine to certain proteins in cutis or nasal mucosa.

Administration, Intranasal↗
PubMed1991

[Apomorphine in Parkinson disease].

28 patients with parkinsonism received the dopamine agonist drug apomorphine for the period August 1990-August 1991. Treatment with repeated subcutaneous injections was started in 13 patients who had suffered from Parkinson's disease for more than ten years. All patients received optimal levodopa treatment. Apomorphine had a very good effect in eight patients; i.e. the time in offphase was markedly reduced. This very good effect was seen only in patients with marked on-off phenomena and usually end of dose failure. The patients who experienced the best effect had little dyskinesias during on-phase and were not mentally affected. An additional 15 patients were given apomorphine for diagnostic purposes. Following a positive test, levodopa treatment was started in one patient and the levodopa dose was increased in two others. In the remaining patients the apomorphine test was negative, and levodopa treatment was not reinstituted.

Aged↗
PubMed1991

Effects of apomorphine, a dopamine receptor agonist, on ocular refraction and axial elongation in a primate model of myopia.

The authors examined the effect of local administration of a dopamine receptor agonist on visual deprivation-induced excessive ocular growth and myopia. Eight rhesus monkeys were monocularly deprived of vision from birth with opaque contact lenses. Four of the monkeys received drops of 1% apomorphine HCl 2-3 times/day in the occluded eye; the four control monkeys received vehicle only. Axial lengths were determined by A-scan ultrasonography at birth and at 5-7 months of age. The authors assessed the axial elongation by comparing the postnatal growth in the axial dimension of the occluded eyes with the postnatal growth in nonoccluded eyes. In three of the four control monkeys, occlusion increased axial growth by an average of 1.3 mm. In contrast, they found that growth of the occluded and nonoccluded eyes of the apomorphine-treated monkeys was equivalent, except in one monkey whose nonoccluded eye did not develop normally and was anomalously small. At 6.5-9.5 months of age, three of four controls had myopic refractive errors (-3 to -7 diopters) in the occluded eyes; three of four of the apomorphine-treated monkeys had hyperopic refractive errors (+1-(+)3 diopters) in their occluded eyes. The occluded eye of the fourth monkey was only -0.5 diopters myopic. The findings suggest that apomorphine administration retards excessive axial elongation and the concomitant development of myopia associated with visual deprivation in primates.

Administration, Topical↗
PubMedDate not supplied

[The apomorphine test for diagnosis of parkinsonian syndrome].

Apomorphine is a powerful dopaminergic drug, able to improve cardinal symptoms of Parkinson's disease in few minutes, when injected subcutaneously. We administered different doses of apomorphine s.c. against placebo in 25 patients with a Parkinsonian syndrome, with the aim of discriminating Parkinson's disease from other Parkinsonism. A positive response to apomorphine was predictive (88%) of good responsiveness to levodopa therapy. Our data, together with those of other groups, indicate that apomorphine test is a useful tool in the diagnosis of Parkinsonian syndromes.

Aged↗
PubMed1989

One trial conditioning with apomorphine is blocked by cycloheximide.

Rats with unilateral 6-hydroxydopamine lesions of substantia nigra were treated with 0.05 mg/kg apomorphine and observation of their circling behavior was made. Twenty minutes after the apomorphine treatment they were injected with saline or 2 mg/kg cycloheximide. Two weeks after drug treatment, control animals exhibited rapid contralateral rotation in response to being placed in the rotation environment. This conditioned rotation was not observed in cycloheximide-treated animals. After the first test trial animals received a second apomorphine administration, this time followed by saline injection in both groups. Subsequent to the second apomorphine treatment both groups showed conditioned rotation.

Animals↗
PubMedDate not supplied

Stability and variability of locomotor responses of laboratory rodents. IV. The responses of rats and mice to apomorphine and amphetamine.

Both apomorphine and amphetamine produce hypermotility in mice and rats previously adapted to the measuring apparatus. The amphetamine hypermotility, induced by 1.5 mg/kg ip of the drug, began to develop after 20 min and lasted for over 1 h. The response was similar in animals tested at various times of the year. In the investigated populations approx. 20% of rats were very highly stimulated, and approx. 15% did not respond with hypermotility. The individual response was a stable feature of a given rat, as the correlation of results of subsequent tests was significant. Apomorphine (1 mg/kg sc) stimulates the locomotor activity of the rat immediately after the injection. The seasonal variability of response was high. The results of subsequent tests were correlated. The differences between animals were less distinct than those observed after amphetamine. In mice hypermotility induced by apomorphine (1 mg/kg sc) began to evolve after 10 min, the amphetamine hypermotility - after 40 min. There exist subpopulations reacting very strongly to either of the drug. The responses in subsequent tests were well correlated. In mice the second injection of amphetamine (after 4 days) produced a much higher locomotor response than the first injection, while in all other cases (apomorphine in mice, both dopaminomimetics in rats) the magnitude of responses in subsequent tests was similar. No correlations between the type of responses to the drugs and characteristics of central catecholaminergic receptors were found.

Amphetamine↗
PubMed1985

Effect of a novel environment on locomotor hyperactivity of rats induced by apomorphine in the nucleus accumbens.

Bilateral local injections into the nucleus accumbens of apomorphine in doses between 0.125 and 20 micrograms produced a dose-dependent increase of locomotor activity in rats recorded over the first 5-min period after placing the animals in a novel environment 7 min after the injection. Continuous records over consecutive 5-min periods revealed that the locomotor effect of apomorphine (1 microgram, bilaterally) declines rapidly within less than 30 min. Progressively weaker locomotor hyperactivity in the first 5-min periods was observed after prolongation of the interval between intra-accumbens injection of apomorphine and the commencement of testing from 7 to 12, 17 and 22 min, respectively. Since no difference was found between locomotor activity of animals just placed in the novel environment and that of animals already present in this environment for one or more periods of record at fixed times after the injection, it is concluded that exploration does not contribute to locomotor hyperactivity induced by intra-accumbens injections of apomorphine.

Animals↗
PubMed1975

The effect of various chlorpromazine derivatives on the apomorphine-elicited inhibition of synaptosomal tyrosine hydroxylase activity.

The effects of chlorpromazine and of some metabolites of chlorpromazine on the apomorphine-elicited inhibition of synaptosomal tyrosine hydroxylase activity were investigated. Chlorpromazine, nor1-chlorpromazine and 7-hydroxychlorpromazine reverse the apomorphine-elicited inhibition of tyrosine hydroxylase activity while nor1-chlorpromazine sulfoxide and nor2-chlorpromazine sulfoxide have no effect on this inhibition. 6-Hydroxychlorpromazine and promethazine also reverse the enzyme inhibition by apomorphine but are less potent than chlorpromazine or 7-hydroxychlorpromazine. These results show that chlorpromazine and its metabolites with antipsychotic activity are more effective in reversing the apomorphine-elicited inhibition of tyrosine hydroxylase than those metabolites which are devoid of antipsychotic activity.

Animals↗