MAO blocker

MAO inhibitors can be classified as simple indole alkaloids (e.g., 13-carbolines, N,N-dimethyltryptamine N-methyltryptamine), simple isoquinolines (carnegine, salsolidine, salsolinol), quinoline alkaloids (e.g., quinine) and even complex indole alkaloids (e.g., vinblastine and vincristine). A structural similarity can be seen between the MAO blocker and endogenous substrates between the indole alkaloids and serotonin between the simple isoquinoline and dopamine, noradrenaline and adrenaline, which implies that these compounds bind to the active site of the enzyme. 

In addition to halopeiidol, the putative neuroleptics, limcazole (311), lemoxipiide (312), and gevotioline (313) bind to (7-ieceptois as does the dopamine uptake blocker, GBR 12909 (314) and two ligands active at the NMDA receptor, ifenprodil (315) and CNS 1102 (316). NPC 16377, (317) is a selective (7-teceptor ligand. MAO inhibitors and antidepressants also bind to (7-teceptors. Some evidence indicates that (7-teceptors in the brain are in fact a form of cytochrome which may account for the diversity of ligands interacting with (7-sites. 

Drugs that may affect nasal decongestants include beta blockers, furazolidone, guanethidine, methyidopa, MAO inhibitors, rauwolfia alkaloids, tricyclic antidepressants, urinary acidifiers, and urinary alkalinizers. 

Drugs that may affect antihistamines include aluminum/magnesium-containing acids, cimetidine, erythromycin, ketoconazole, MAO inhibitors, and rifamycins (eg, rifampin). Drugs that may be affected by antihistamines include alcohol and CNS depressants, beta-blockers, MAO inhibitors, metyrapone, nefazodone, selective serotonin reuptake inhibitors (SSRIs), and venlafaxine. 

Drugs that may affect barbiturates include alcohol, charcoal, chloramphenicol, MAO inhibitors, rifampin, and valproic acid. Drugs that may be affected by barbiturates include acetaminophen, anticoagulants, beta blockers, carbamazepine, chloramphenicol, clonazepam, oral contraceptives, corticosteroids, digitoxin, doxorubicin, doxycycline, felodipine, fenoprofen, griseofulvin, hydantoins, methoxyflurane, metronidazole, narcotics, phenmetrazine, phenylbutazone, quinidine, theophylline, and verapamil. 

Sulfonamides Chloramphenicol Probenecid Coumarins MAO inhibitors Beta-blockers... 

Drug interactions NSAIDs Salicylates Sulfonamides Chloramphenicol Probenecid Coumarins MAO inhibitors Beta-blockers Thiazides and other diuretics Corticosteroids Phenothiazines Thyroid products Estrogens Oral contraceptives Phenytoin Nicotinic acid Sympathomimetic Calcium channel blockers Isoniazid Miconazole... 

As social phobia is only recently becoming better recognized and researched, better documentation for the various treatments mentioned above is now evolving. This applies especially to the five SSRIs and to some of the newer antidepressants such as venlafaxine XR. Guidelines are emerging for the use of high-potency benzodiazepines, MAO inhibitors, RIMAs, beta blockers, and various drugs in combination as second- or third-line treatments for social phobia. 

Recall that depression is a notable source of secondary negative symptoms, and NE is a neurotransmitter of interest in depression. This could potentially complicate investigation into NE and negative symptoms unless patients were specifically examined for deficit symptoms. This may help explain the mixed results of treating negative symptoms with NE blockers, reuptake inhibitors, and MAO inhibitors (as reviewed by Buchanan et al., 1996 Carpenter et al., 2000 Bodkin et al., 2005). 

MAO inhibitors can cause bradycardia. A report of two cases of interactions of monoamine oxidase inhibitors with beta-blockers (nadolol and metoprolol) is of interest, and several possible mechanisms were discussed (14). 

Interactions. With nonselective monoamine oxidase inhibitors (MAOI), the monoamine dopamine formed from levodopa is protected from destruction it accumulates and also follows the normal path of conversion to noradrenaline (norepinephrine), by dopamine (J-hydroxylase severe hypertension results. The interaction with the selective MAO-B inhibitor, selegiline, is possibly therapeutic (see below). Tricyclic antidepressants are safe. Levodopa antagonises the effects of antipsychotics (dopamine receptor blockers). Some antihypertensives enhance hypotensive effects of levodopa. Metabolites of dopamine in the urine interfere with some tests for phaeochromocytoma, and in such patients it is best to measure the plasma catecholamines directly. 

Enzyme inhibition. Ciprofloxacin and cimetidine inhibit hepatic metabolism of lipid-soluble J-adrenoceptor blockers, e.g. metoprolol, labetalol, propranolol, increasing their effect. Methyldopa plus an MAO inhibitor may cause excitement and hallucinations. 

Clinically important, potentially hazardous interactions with aminophylline, beta-blockers, MAO inhibitors, tricyclic antidepressants... 

Clinically important, potentially hazardous interactions with albuterol, alpha-blockers, amitriptyline, amoxapine, atenolol, beta-blockers, carteolol, chlorpromazine, clomipramine, cocaine, desipramine, doxepin, ephedra, ergotamine, furazolidone, halothane, imipramine, insulin detemir, MAO inhibitors, metoprolol, nadolol, nortriptyline, oxprenolol, penbutolol, phenelzine, phenoxybenzamine, phenylephrine, pindolol, prazosin, propranolol, protriptyline, sympathomimetics, terbutaline, thioridazine, timolol, tranylcypromine, tricyclic antidepressants, trimipramine, vasopressors... 

Clinically important, potentially hazardous interactions with acetazolamide, aminoglycosides, anticholinesterases, bambuterol, calcium channel blockers, chloroquine, chlorpromazine, clindamycin, d-pencillamine, ecothiophate iodine, enflurane, furosemide, halothane, hexomethonium, isoflurane, ketamine, lidocaine, lincomycin, lithium salts, magnesium salts, mannitol, MAO inhibitors, organophosphates, pancuronium, phenytoin, polymyxins, procainamide, quinidine, sevoflurane, spectinomycin, tetracyclines... 

Zhang Y, Gupta A, Wang H, Zhou L, Vethanayagam RR, Unadkat JD, Mao Q (2005) BCRP transports dipyridamole and is inhibited by calcium channel blockers. Pharm Res 22 2023-2034... 

Adrenaline is contraindicated in cases of diabetes, hyperthyroidism, serious heart arrhythmias and coronary insufficiency or in combination with beta-blockers or monoamine oxidase (MAO) inhibitors. Lidocaine with adrenaline has a very rapid onset of action. Its duration of action is longer than that of lidocaine without adrenaline. However, inadvertent injection of a lidocaine-adrenaline solution into the vessels located near the nerve trunks increases the heart rate (immediate sinus tachycardia at over 130 beats per minute, spontaneously reversible in around 15 minutes) and increases ventricular excitability (risk of fibrillation). It can trigger angina attacks that may lead to a heart attack. It is therefore preferable not to use adrenaline before a full-face phenol peel. 

Muscarinic receptor blockers may improve muscle rigidity and tremor in Parkinsons disease but result in very little improvement in bradykinesia thus, they are mainly considered as adjunctive to the use of drugs that improve dopaminergic function. Selegiline is the inhibitor of MAO type B, and pramipexole is a non-ergot DA receptor agonist. Carbidopa inhibits peripheral AAAD (dopa decarboxylase) tolcapone is an inhibitor of COMT. Levodopa causes a high incidence of dose-dependent dyskinesias that are not slow in onset, like tardive dyskinesia that results from chronic administration of DA receptor blockers. 

The drug is not significantly affected by MAO, but it is 3-methylated by COMT in the lung and other extraneural tissue. Frequently, repeated administration can lead to fastness or a loss of bronchodilating effect, which may in part be due to the accumulating 3-methoxy metabolite, a weak (3-blocker theoretically capable of causing broncho-constriction. In any case, IPR has become the prototype compound against which all the newer bronchodilators are compared. 

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