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Anti phenobarbital

Malone J, Sullivan MA (1996) Analysis of antibody selection by phage display utilizing anti-phenobarbital antibodies. J Mol Recognit 9 738-745. [Pg.722]

The interaction of ketamine with each of the three anticonvulsant compounds was also tested. Ketamine, 15 mg/kg, a dose showing no anti-PTZ effect and causing no overt behavioral changes, potentiated the effect of phenobarbital (20 mg/kg) in delaying the clonic and tonic convulsive responses and lethality (figure 3). Ketamine also potentiated the ability of phenytoin (20 mg/kg) to delay... [Pg.82]

The results demonstrate anticonvulsant properties of PCP and ketamine in two quite different seizure models. On the one hand, ketamine was effective in antagonizing several components of PTZ activity. Others have previously reported anti-PTZ effects of ketamine. However, the present results demonstrate that the anticonvulsant effects of ketamine against PTZ seizures closely resembled the effects of phenobarbital in that both compounds delayed clonic convulsions and prevented tonic extension. Moreover, a low dose of ketamine, which alone showed no anticonvulsant effect or overt behavioral changes, potentiated the anti-PTZ effects of phenobarbita 1. These findings suggest that ketamine possesses selective anticonvulsant properties. The anticonvulsant mechanism of action for phenobarbital is not known. However, the similarities between ketamine and phenobarbital, and the interaction between the two compounds, suggest a common mechanism or site of acti on. [Pg.89]

A potentially powerful probe for sorting out the contribution of hydroperoxide-dependent and mixed-function oxidase-dependent polycyclic hydrocarbon oxidation is stereochemistry. Figure 9 summarizes the stereochemical differences in epoxidation of ( )-BP-7,8-dihydrodiol by hydroperoxide-dependent and mixed-function oxidase-dependent pathways (31,55,56). The (-)-enantiomer of BP-7,8-dihydrodiol is converted primarily to the (+)-anti-diol epoxide by both pathways whereas the (+)-enantiomer of BP-7,8-dihydrodiol is converted primarily to the (-)-anti-diol epoxide by hydroperoxide-dependent oxidation and to the (+)-syn-diol epoxide by mixed-function oxidases. The stereochemical course of oxidation by cytochrome P-450 isoenzymes was first elucidated for the methycholanthrene-inducible form but we have detected the same stereochemical profile using rat liver microsomes from control, phenobarbital-, or methyl-cholanthrene-induced animals (32). The only difference between the microsomal preparations is the rate of oxidation. [Pg.323]

Primidone is an other second line barbiturate used orally to control tonic-clonic and partial seizures. It is a pro-drug as it is metabolized to phenobarbital and phenylethylmalonamide (PEMA), however both the parent compound as well as the metabolites have anti seizure activity. Its use is more difficult to monitor and adverse effects occur even more frequently than with phenobarbital. [Pg.356]

Evening Primrose Oil (Oenof/iera biennis) Uses PMS, diabetic neuropathy, ADHD, IBS, RA, mastalgia Action Anti-inflammatory, antispas-modic, diuretic, sedative effects related to a high concentration of essential fatty acids esp GLA CLA their conversion into prostaglandins Available forms Caps, gel-caps, Liq dose depends on GLA content DM neuropathy 4000-6000 mg PO OD Eczema 4000 mg PO OD Mastalgia 3000 1000 mg PO -r doses PMS 2000-4000 mg PO OD RA Up to 5000 mg PO OD Notes/SE Indigestion, N, soft stools, flatulence, HA, anorexia, rash Contra Do not use PRG or lactation do not use persons w/ Sz disorders Interactions T Phenobarbital metabolism, i Sz threshold, T effects OF diuretics, sedatives EMS May take up to 4 mo for max effectiveness T risk of Szs... [Pg.329]

By 1912, von Mering and Fischer developed and commercially introduced a new barbiturate compound for sleep and anxiety called phenobarbital or Luminal. However, this medication quickly found its place as treatment for a very different medical condition, epilepsy, which is a condition of periodic, unprovoked convulsions or seizures. The main goal of epilepsy treatment is to decrease the frequency of seizures. Alfred Hauptmann discovered the anti-epileptic properties of phenobarbital accidentally. A 1912 report by Hauptmann described epileptic patients who were given phenobarbital for sedation and incidentally had fewer seizures. Seizures are caused by an abnormal impulse in the brain, which spreads and sends inappropriate message to the body. These messages result in... [Pg.32]

APREPITANT ANTI EPILEPTICS -CARBAMAZEPINE, PHENOBARBITAL, PHENYTOIN 1 aprepitant levels Induction of CYP3A4-mediated metabolism of aprepitant Watch for poor response to aprepitant... [Pg.203]

CARMUSTINE ANTIEPILEPTICS -PHENOBARBITAL 1 plasma concentrations of carmustine and 1 anti-tumour effect in animal experiments Attributed to induction of liver metabolizing enzymes of carmustine by phenobarbitone, particularly with long-term therapy Avoid concurrent use. As this study did not show any interaction with phenytoin, phenytoin may be a suitable alternative antiepileptic... [Pg.293]

IFOSFAMIDE 1. ANTIBIOTICS-rifampicin 2. ANTICANCER AND IMMUNOMODULATING DRUGS - dexamethasone 3. ANTIDEPRESSANTS-St John s wort 4. ANTI EPILEPTICS -carbamazepine, phenytoin, phenobarbital t rate of biotransformation to 4-hydroxyifbsfamide, the active metabolite, but there is no change in AUC of 4-hydroxyifosfamide Due to t rate of metabolism and of clearance owing to induction of CYP3A4 and CYP2D6 Be aware - clinical significance may be minimal or none... [Pg.308]

Drugs. Antiepilepsy drugs, particularly phenytoin, primidone and phenobarbital, occasionally cause a macrocytic anaemia that responds to folic acid. This may be due to enzyme induction by the antiepileptics increasing the need for folic acid to perform hydroxylation reactions (see Epilepsy) but other factors such as reduced absorption may be involved. Administration of folic acid causes a recurrence of seizures in some patients. Some anti-malarials, e.g. pyrimethamine, may interfere with conversion of folates to the active tetrahydrofolic acid, causing macrocytic anaemia. Methotrexate, another folate antagonist, may cause a megaloblastic anaemia especially when used long-term for leukaemia, rheumatoid arthritis or psoriasis. [Pg.597]

Clinically important, potentially hazardous interactions with allopurinol, amiodarone, amobarbital, anabolic steroids, anti-thyroid agents, aprobarbital, aspirin, barbiturates, bivalirudin, butabarbital, butalbital, cimetidine, clofibrate, clopidogrel, cyclosporine, delavirdine, disulfiram, fenofibrate, fluconazole, gemfibrozil, glutethimide, imatinib, itraconazole, ketoconazole, levothyroxine, liothyronine, mephobarbital, methimazole, metronidazole, miconazole, penicillins, pentobarbital, phenobarbital, phenylbutazones, piperacillin, prednisone, primidone, propylthiouracil, quinidine, quinine, rifabutin, rifampin, rifapentine, rofecoxib, salicylates, secobarbital, sulfinpyrazone, sulfonamides, testosterone, thyroid, zileuton... [Pg.178]

Tiagabine has an elimination half-Ufe of 7 to 9 hours. In patients receiving CyP 3A4 inducing anti-epileptic drugs (AEDs), the elimination half-life decreases to 4 to 7 hours. Phenytoin, phenobarbital, and carbamazepine are CyP 3A4 inducers. Valproic acid and gabapentin are not. Tiagabine is not considered to be a CyP 3A4 inducer. ... [Pg.1255]

Krnjevic and Videk ) described a new screening test based on a "natural reaction of a rat, namely the entrance into a darkened cage through a hole of suitable size (5 cm. ). Either of several depressants, chlorpromazine, reserpine, phenobarbital, etc. increased the time required for this reaction. A pyschostimulant, amphetamine, decreased the time, as did the anti-depressants imipramine or nialamide. [Pg.24]

Phylloquinone, menaquinone, and menaphthone have been extracted from serum into supercritical CO2 and separated with SFC, with detection at 250 nm (127). Serum, supported on celite, was transferred to extraction cartridges and extracted with supercritical CO2 at 45°C prior to the analysis of benzodiazepines, anabolic agents, and nonsteroidal anti-inflammatory drugs by HPLC (128). Phenobarbital, butalbital, pentobarbital, and thiopental have been extracted from human serum prior to liquid chromatography-negative-ion electrospray tandem mass spectrometry analysis (129). The sample was extracted with supercritical CO2 at 40°C and 507 bar with static extraction for 5 min followed by dynamic extraction for 30 min. Calibrations graphs were linear for 1-60 pg/mL of each barbiturate and the detection limits were 23, 25, 50, and 225 ng/mL of thiopental, pentobarbital, butalbital, and phenobarbital, respectively. In the determination of the cited analytes in serum spiked at the 10- and 50-pg/mL levels, the recoveries were 94.2-106.9% and the RSDs were 1.14-5.18% (three replicates). [Pg.562]

Active as anti-tumor promoter on two-stage carcinogenesis test of mouse hepatic tumor using N-nitrosodiethylamine and phenobarbital ... [Pg.371]


See other pages where Anti phenobarbital is mentioned: [Pg.339]    [Pg.1164]    [Pg.99]    [Pg.101]    [Pg.13]    [Pg.99]    [Pg.186]    [Pg.254]    [Pg.329]    [Pg.332]    [Pg.102]    [Pg.1164]    [Pg.1075]    [Pg.68]    [Pg.11]    [Pg.73]    [Pg.99]    [Pg.186]    [Pg.332]    [Pg.604]    [Pg.50]    [Pg.258]    [Pg.697]    [Pg.697]    [Pg.3350]    [Pg.3963]    [Pg.257]    [Pg.174]    [Pg.193]    [Pg.127]    [Pg.212]    [Pg.11]   
See also in sourсe #XX -- [ Pg.237 , Pg.268 , Pg.273 , Pg.278 , Pg.281 , Pg.284 ]




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Phenobarbital

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