Effects of amantadine on circulating neurotransmitters in healthy subjects

Lechín, Fuad; Dijs, Bertha van der; Pardey-Maldonado, Betty; Rivera, Jairo E; Baez, Scarlet; Lechin, Marcel E.

doi:10.1007/s00702-010-0371-1

Cited by 13 publications

(12 citation statements)

References 32 publications

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“…The increase of the afterload may be induced by the release of noradrenaline from the peripheral nerve terminals into the vessels (Lechin et al, 2010), and this vasopressor effect was consistent with previous in vivo study of rats (Ikeda et al, 2015). Meanwhile, the cardiac output decreased, but the preload to the ventricle increased, which may suggest that extent of increase in the afterload was greater than that of the ventricular contraction.…”

Section: Cardiohemodynamic Effectssupporting

confidence: 89%

Electropharmacological effects of amantadine on cardiovascular system assessed with J-Tpeak and Tpeak-Tend analysis in the halothane-anesthetized beagle dogs

et al. 2016

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-Since amantadine-induced long QT syndrome has been clinically reported, we investigated its electropharmacological effects to estimate the extent of proarrhythmic risk by using the halothane-anesthetized beagle dogs (n = 4). Amantadine in doses of 0.1, 1 and 10 mg/kg was infused over 10 min with a pause of 20 min under the monitoring of multiple cardiovascular variables. J-T peak and T peak -T end were separately measured on the lead II electrocardiogram to precisely analyze the net balance between inward and outward current modifications by amantadine. The low dose increased the ventricular contractile force, but suppressed the intraventricular conduction. The middle dose prolonged the QT interval besides enhancing the changes induced by the low dose. The high dose increased the mean blood pressure, left ventricular end-diastolic pressure and total peripheral resistance, and accelerated the atrioventricular nodal conduction, but decreased the cardiac output besides enhancing the changes induced by the middle dose. A reverse use-dependence was confirmed in the repolarization delay. Amantadine hardly affected the J-T peak , but prolonged the T peak -T end . Amantadine can be considered to stimulate Ca 2+ channel but inhibit Na + and K + channels in the in situ heart. J-T peak and T peak -T end analysis suggests that amantadine may possess modest risk for arrhythmia.

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Section: Cardiohemodynamic Effectssupporting

confidence: 89%

Electropharmacological effects of amantadine on cardiovascular system assessed with J-Tpeak and Tpeak-Tend analysis in the halothane-anesthetized beagle dogs

et al. 2016

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“…Exacerbation of this peripheral + CNS interaction underlies the pathophysiology of the Bezold Jarisch syndrome [132][133][134][135]. This disturbance is successfully treated throughout an adequate neuropharmacological therapy, addressed to enhance the neural sympathetic activity which annuls parasympathetic overactivity [12,14,52,54,[136][137][138][139].…”

Section: Physiological Evidencementioning

confidence: 99%

“…We have also investigated the effects induced by different types of drugs: clonidine [9-11], sibutramine [12], buspirone [13], tianeptine [14], arginine [15], doxepin [8], dexamethasone [16,17] on the circulating neurotransmitters of both normal and diseased subjects.…”

Section: Introductionmentioning

confidence: 99%

Central Nervous System Circuitries Underlying Two Types of Peripheral Autonomic Nervous System Disorders~!2008-04-24~!2008-09-26~!2008-12-05~!

Lechín¹,

Dijs²

2008

TONEURJ

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Abstract:The assessment of circulating neurotransmitters: noradrenaline, adrenaline, dopamine, platelet serotonin, plasma serotonin and plasma tryptophan before and after many types of stressor agents and neuropharmacological drugs carried out over the last thirty years allowed us to accumulate information dealing with the central nervous system (CNS) versus the peripheral autonomic nervous system (ANS) interactions in healthy as well as diseased mammals. Furthermore, the accurate knowledge about the CNS circuitry disorders which underlie both the CNS and peripheral clinical syndromes, has allowed us to prescribe successful neuropharmacological therapeutical strategies for many types of illnesses. In addition, the demonstration that the clinical improvement was always paralleled by the normalization of the neurochemical, hormonal, immunological and clinical profiles affords strong support to our point of view. According to all the above, the authors postulate the existence of two types of diseases: type A and Type N, which are underlain by two opposite CNS + ANS disorders. Type A diseases should be associated with the "uncoping stress" syndrome and are underlain by hyperactivity of the adrenocortical glands plus the CNS disorder characterized by the predominance of the C1(adrenergic) + DR(serotonergic) axis over the A5(noradrenergic) + MR(serotonergic) binomial, whereas the type N diseases depends on the opposite profile: "endogenous depression" syndrome. Finally, we quoted exhaustive evidence showing that the well known fading of both the A6(noradrenergic) + C1(adrenergic) CNS nuclei activity occurring during aging is responsible for the ANS + CNS disorder which is similar to that underlying psychosis, Alzheimer, post-traumatic stress disorder and deficit-attention hyperactive disorder.

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“…Methenamine is an adamantane analogue, and in this, the cage-like backbone includes seven carbons and three nitrogens 9. In healthy subjects, amantadine results in an increase in circulating norepinephrine, and a decrease in epinephrine, dopamine and serotonin 10. It is not known whether methenamine has an effect on catecholamine metabolism, but this could be a possible mechanism for the induction of RCVS in this case.…”

Section: Discussionmentioning

confidence: 92%

The reversible cerebral vasoconstriction syndrome in association with venlafaxine and methenamine

et al. 2013

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The reversible cerebral vasoconstriction syndrome (RCVS) is characterised by thunderclap headache and multifocal vasoconstriction of cerebral arteries on angiography. It is often drug induced, but it can occur postpartum, and as a result of a number of other precipitants. To make the diagnosis, it is necessary to exclude other causes of severe headache (such as aneurysmal subarachnoid haemorrhage, carotid dissection and primary angiitis of the central nervous system). However, it is also important to show that the vasoconstriction has resolved with repeat angiography at the 3-month stage. Here we report two cases of RCVS in association with venlafaxine and the urinary antiseptic, methenamine. Serotonin-norepinephrine reuptake inhibitors have recently been reported as a possible precipitant, but this is the first report to implicate methenamine. Although RCVS is relatively uncommon, it should be considered in the differential of those presenting with thunderclap headache.

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Effects of amantadine on circulating neurotransmitters in healthy subjects

Cited by 13 publications

References 32 publications

Electropharmacological effects of amantadine on cardiovascular system assessed with J-T<sub>peak</sub> and T<sub>peak</sub>-T<sub>end</sub> analysis in the halothane-anesthetized beagle dogs

Electropharmacological effects of amantadine on cardiovascular system assessed with J-T<sub>peak</sub> and T<sub>peak</sub>-T<sub>end</sub> analysis in the halothane-anesthetized beagle dogs

Central Nervous System Circuitries Underlying Two Types of Peripheral Autonomic Nervous System Disorders~!2008-04-24~!2008-09-26~!2008-12-05~!

The reversible cerebral vasoconstriction syndrome in association with venlafaxine and methenamine

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