Monoamine oxidase inhibitors nervous system

Synergy of unwanted pharmacological effect ginseng and its products will inhibit the central nervous system (CNS) when they are applied with luminal, chloral hydrate, or ephedrine, which can increase the release of dopamine, noradrenaline, and serotonin in the CNS thus inducing a hypertensive crisis if monoamine oxidase inhibitors (MAOIs) are given simultaneously. 

Urine catecholamines may also serve as biomarkers of disulfoton exposure. No human data are available to support this, but limited animal data provide some evidence of this. Disulfoton exposure caused a 173% and 313% increase in urinary noradrenaline and adrenaline levels in female rats, respectively, within 72 hours of exposure (Brzezinski 1969). The major metabolite of catecholamine metabolism, HMMA, was also detected in the urine from rats given acute doses of disulfoton (Wysocka-Paruszewska 1971). Because organophosphates other than disulfoton can cause an accumulation of acetylcholine at nerve synapses, these chemical compounds may also cause a release of catecholamines from the adrenals and the nervous system. In addition, increased blood and urine catecholamines can be associated with overstimulation of the adrenal medulla and/or the sympathetic neurons by excitement/stress or sympathomimetic drugs, and other chemical compounds such as reserpine, carbon tetrachloride, carbon disulfide, DDT, and monoamine oxidase inhibitors (MAO) inhibitors (Brzezinski 1969). For these reasons, a change in catecholamine levels is not a specific indicator of disulfoton exposure. 

M, metaboiism S, at or near site of action IV, intravenously MHS, malignant hyperthermia syndrome ALA, aianine ICU, intensive care unit CNS, central nervous system MAOI, monoamine oxidase inhibitor, NSAID, non-steroidal anti-inflammatory drug ACE, angiotensin in-converting enzyme 5-HT, 5-hydrox ryptamine. 

Blier P, de Montigny C, Azzaro AJ. Modification of serotonergic and noradrenergic neurotransmissions by repeated administration of monoamine oxidase inhibitors Electrophysiological studies in the rat central nervous system. J Pharmacol Exp Ther 1986 237 987-994. 

Drugs and chemicals are known to cause activated interaction. The depressant action of opioid drugs is enhanced by drugs acting on the central nervous system (CNS) such as alcohol, anesthetics, anxiolytics, hypnotics, tricyclic antidepressants, and antipsychotics. Concomitant administration of opioid analgesics and monoamine oxidase inhibitors (MAOIs) should be avoided, or extra care should be taken if such a therapy is inevitable. Fatal reactions are reported when treated along with selegiline. Interactions also are reported with cyclizine, cimetidine, mexiletine, cisapride, metoclopramide, or domperidone. 

Opioid analgesics interact with non-selective monoamine oxidase inhibitors, causing nervous system excitation and hypertension (70). These interactions have been reviewed (SEDA-18, 14). 

Concomitant use of some opioid analgesics, such as pethidine or dextropropoxyphene, with the selective monoamine oxidase inhibitors selegiline and moclobe-mide can enhance their nervous system toxicity (71). 

NERVOUS SYSTEM DRUGS ANTIDEPRESSANTS Monoamine oxidase inhibitors... 

LINEZOLID - Drugs Acting on the Nervous System, Antidepressants, Monoamine oxidase inhibitors ... 

Interactions. Morphine (also pethidine and possibly other opioids) is potentiated by monoamine oxidase inhibitors. Any central nervous system depressant (including alcohol) will have additive effects. Patients recently exposed to neuromuscular blocking agents (unless this is adequately reversed, e.g. by neostigmine) are particularly at risk from the respiratory depressant effects of morphine. The effect of diuretic drugs may be reduced by release of antidiuretic hormone by morphine. Useful interactions include the potientating effect on pain relief of tricyclic antidepressants and of dexamfetamine. 

Anorectic drugs, which are structurally related to the amphetamines, act mainly on the satiety centre in the hypothalamus and also increase general physical activity (1). All of them, except fenfluramine, stimulate the central nervous system and can cause restlessness, nervousness, irritabihty, and insomnia. Adverse effects also occur through sympathetic stimulation and gastrointestinal irritation. Drug interactions can occur with monoamine oxidase inhibitors. Dexamfetamine, phenmetrazine, and benzfetamine can cause dependence. Some of them have been associated with cardiac valvulopathy and primary pulmonary hypertension (2). 

MONOAMINE-OXIDASE-INHIBITORS(MAOIs) acton monoamine-oxidase (MAO) enzymes that are involved in the degradation of monoamines in the peripheral and central nervous system. Monoamine oxidase occurs within cells bound to the surface of the mitochondria. It is found not only within monoaminergic neurons, but also in the liver and intestinal epithelium. The enzyme converts amines to their corresponding aldehydes, which in the periphery are converted to their carboxylic acids by aldel e dehydrogenase. Neurotransmitters degraded by monoamine oxidase include dopamine. 5-hydnngrtryptamine and noradrenaline. 

CNS, central nervous system DA, dopamine 5-HT, serotonin LSD, lysergic acid diethylamide MAOl, monoamine oxidase inhibitor NE, norepinephrine PCP, phencyclidine ... 

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