Tramadol

Tramadol has about one tenth the pain-relieving ability of morphine.53 There are two enantiomers, and both contribute to pain relief, but via different mechanisms. (+)-Tramadol and the metabolite (+)-0-desmethy 1-tramadol, which is referred to as Ml, are agonists of the mu opioid receptor. (+)-Tramadol inhibits serotonin reuptake and (-)-tramadol inhibits norepinephrine re uptake.25 This latter action enhances the inhibitory effects on pain transmission in the spinal cord. Because the actions of the two enantiomers are complementary, they are usually supplied as a racemic mixture. However, because it is a serotonin-reuptake blocker, interaction with other medications can lead to the occurrence of serotonin syndrome.54 

Tramadol is available as drops, capsules, and sustained-release formulations for oral use, suppositories for rectal use, and solution for intramuscular, intravenous, and subcutaneous injection. After oral administration, tramadol is rapidly and almost completely absorbed. Sustained-release tablets release the active ingredient over a period of 12 h, reach peak concentrations after 4.9 h, and have a bioavailability of 87 to 95% compared with capsules. One 100-mg dose given to healthy volunteers resulted in plasma levels of 375 ng/ml at 1.5 h.55 Tramadol is 20% bound to plasma protein and it is rapidly distributed in the body it is mainly metabolized by O- and A-demethylation forming glucuronides and sulfates that are excreted by the kidney. 

The mean elimination half-life is about 6 h. The O-demethylation of tramadol to Ml, the main analgesic effective metabolite, is catalyzed by cytochrome P450 (CYP) 2D6, whereas A-demeth-ylation to M2 is catalyzed by CYP2B6 and CYP3A4. The wide variability in the pharmacokinetic properties of tramadol can partly be ascribed to CYP polymorphism. O- and A-demethylation of tramadol as well as renal elimination are stereoselective.56 

Pharmacokinetic—pharmacodynamic characterization of tramadol is difficult because of differences between tramadol concentrations in plasma and at the site of action, and because of pharmacodynamic interactions between the two enantiomers of tramadol and its active metabolites.53 

Tramadol is a pain reliever (analgesic). Its action is similar to opioid narcotics such as codeine and morphine, but it does not depress breathing the way the others can, and less often leads to abuse and addiction. 

Tramadol is an alkaloid, with an amine group (where the nitrogen atom is), which puts it in a group of bitter plant chemicals that often have potent biological activity. 

Alkaloids range from the belladonna alkaloids, such as atropine and scopalomine—which are used as poisons, cold remedies, and truth serums —to dextromethorphan, a cough suppressant (anti-tussive). But the most widely known alkaloids are the opiates, such as morphine, heroin, fentanyl, oxycodone, and methadone. These act on 

Acetylsalicylic acid is more commonly known as aspirin. It is used as a pain reliever, fever reducer, and anti-inflammatory. 

Acetylsalicylic acid breaks down into salicylic acid 20 minutes after entering the bloodstream. It is the salicylic acid that is responsible for the beneficial effects of aspirin. Salicylic acid itself is too caustic to be taken orally. 

Guard column 15 X 3.2 7 pm Applied Biosystems pre-column Column 100 X 2 10 pm pPorasil 

Mobile phase MeCN 5 mM pH 3.75 sodium acetate 80 20 Flow rate 1 Injection volume 200 Detector UV 214 

Simultaneous buprenorphine, butorphanol, codeine, ethylmorphine, fentanyl, morphine, nalbuphine 

Noninterfering atropine, diazepam, neostigmine, pancuronium, succinylcholine, thiopental 

Determination of buprenorphine by high-performance hquid chromatography with fluorescence detection application to human and rabbit pharmacokinetic studies. J.Chromatogn, 1991, 570, 339-350 

Apart from Valoron N , this substance is the only centrally active analgesic that is not prohibited by the BtmW. Abusers are sometimes found among medicament-dependent patients who additionally consume other substances such as peripherally active analgesics, benzodiazepines or antidepressants. This substance is not common in the drug scene, and frequency of abuse shows large regional variations. 

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Timolol maleate a-Bromoacetophenone Nomifensine maleate Bromoacetyl bromide Bromazepam Cephapirin sodium Clonazepam Flunitrazepam 5-Bromoacetyl salicylamide Labetalol HCI m-Bromoanisole Tramadol HCI p-Bromoanisole Cyclofenil Bromobenzene... 

Cavoy E., Deltent M. E, Lehoucq S., Miggiano D. (1997) Laboratory-Developed Simulated Moving Bed for Chiral Drug Separations. Design of the System and Separation of Tramadol Enantiomers, J. Chrotnatogr. A 769 49-57. 

Alfentanil, codein, dihydromorphine, etor-phine, fentanyl, heroin, hydromorphone, levo-methadone, morphine, oxycodone, pethidine, piritramide, remifentanil, sufentanil, tilidine, tramadol Buprenorphine, pentazocine Naloxone, naltrexone... 

Trama AbZ (AbZ-Pharma) Trama beta (betapharm) Tramadol (ASTA Medica AWD Dolorgiet ratiopharm Stada ct-Arzneimittel)... 

Cj]HyBrMgO 38046-82-1) see Naproxen (5)-2-(5-bromo-6-methoxy-2-naphthyl)propanoic acid (Ci4Hi BrO 84236-26-0) see Naproxen bromo(3-methoxyphenyl)magnesium (C7H7BrMgO 36282-40-3) see Tramadol (/f)-2-bromo-A -[2-(4-methoxyphenyl)-l-methylethyl]-acetamide... 

Tramadol a weak opioid that also blocks the reuptake of NA and 5-HT—these combined actions synergise to give a good analgesia that lacks some of the typical opioid side-effects. 

Isolated seizures that are not epilepsy can be caused by stroke, central nervous system trauma, central nervous system infections, metabolic disturbances (e.g., hyponatremia and hypoglycemia), and hypoxia. If these underlying causes of seizures are not corrected, they may lead to the development of recurrent seizures I or epilepsy. Medications can also cause seizures. Some drugs that are commonly associated with seizures include tramadol, bupropion, theophylline, some antidepressants, some antipsy-chotics, amphetamines, cocaine, imipenem, lithium, excessive doses of penicillins or cephalosporins, and sympathomimetics or stimulants. 

Glucosamine, tramadol, opioids, topical capsaicin, intraartic-ular corticosteroids, and surgery may be beneficial in certain situations. 

Tramadol is a reasonable option for patients with contraindications to NSAIDs or failure to respond to other oral therapies. For the treatment of hip or knee OA, tramadol is as effective as NSAIDs. The addition of tramadol to NSAIDs or acetaminophen may augment the analgesic effects of a failing regimen, thereby securing sufficient pain relief in some patients. Moreover, concomitant tramadol may permit the use of lower NSAID doses. 

Dizziness, vertigo, nausea, vomiting, constipation, and lethargy are all relatively common adverse events. These effects are more pronounced for several days after initiation and following upward dose titration. Seizures have been reported rarely the risk is dose-related and appears to increase with concomitant use of antidepressants, such as tricyclic antidepressants or selective serotonin reuptake inhibitors. Tramadol should be avoided in patients receiving monoamine oxidase (MAO) inhibitors because tramadol inhibits the uptake of norepinephrine and serotonin. 

Microencapsulation and characterization of tramadol-resin complexes. Journal of Controlled Release, 66, 107-113. 

Y. F. Sha, S. Chen, G. L. Duan, Rapid determination of tramadol in human plasma by headspace solid phase microextraction and capillary gas chromatography mass spectrometry, J. Pharrn. Biomed. Anal., 37, 143 147 (2005). 

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