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Beta blockers interaction with other drugs

Beta blockers may also be involved in pharmacodynamic interactions with other drugs that are based on enhancement or antagonism of pharmacological effects (such as additive blood pressure reduction). [Pg.833]

Other drugs that may interact with cardiac glycosides include the following Albuterol, amphotericin B, beta-blockers, calcium, disopyramide, loop diuretics, nondepolarizing muscle relaxants, potassium-sparing diuretics, succinylcholine, sympathomimetics, thiazide diuretics, thioamines, and thyroid hormones. [Pg.408]

Drug interactions Proleukin may affect central nervous system function. Therefore interactions could occur following concomitant administration of psychotropic drugs. Concurrent administration of drugs possessing nephrotoxic, myelotoxic, cardiotoxic, or hepatotoxic effects with Proleukin may increase toxicity in these organ systems. Reduced kidney and liver function secondary to Proleukin treatment may delay elimination of concomitant medications and increase the risk of adverse events from those drugs. Beta-blockers and other antihypertensives may potentiate the hypotension seen with Proleukin. [Pg.201]

Currently there is a trend toward the synthesis and large-scale production of a single active enantiomer in the pharmaceutical industry [61-63]. In addition, in some cases a racemic drug formulation may contain an enantiomer that will be more potent (pharmacologically active) than the other enantiomer(s). For example, carvedilol, a drug that interacts with adrenoceptors, has one chiral center yielding two enantiomers. The (-)-enantiomer is a potent beta-receptor blocker while the (-i-)-enantiomer is about 100-fold weaker at the beta-receptor. Ketamine is an intravenous anesthetic where the (+)-enantiomer is more potent and less toxic than the (-)-enantiomer. Furthermore, the possibility of in vivo chiral inversion—that is, prochiral chiral, chiral nonchiral, chiral diastereoisomer, and chiral chiral transformations—could create critical issues in the interpretation of the metabolism and pharmacokinetics of the drug. Therefore, selective analytical methods for separations of enantionmers and diastereomers, where applicable, are inherently important. [Pg.624]

Direct information seems to be limited to this study but what occurred is consistent with the way indometacin reduces the effects of many other different antihypertensives (e.g. see ACE inhibitors + NSAIDs , p.28, and Beta blockers + Aspirin or NSAIDs , p.835). It apparently does not affect every patient. If indometacin is added to established treatment with prazosin, be alert for a reduced antihypertensive response. It is not known exactly what happens in patients taking both drugs long-term, but note that with other interactions between antihypertensives and NSAIDs the effects seem to be modest. The manufacturers say that prazosin has been given with indometacin (and also aspirin and phenylbutazone) without any adverse interaction in clinical experience to date. Other manufacturers also... [Pg.88]

This section is mainly concerned with the class I antiarrhythmics, which also possess some local anaesthetic properties, and with class IH antiarrhythmics. Antiarrhythmics that fall into other classes are dealt with under beta blockers , (p.833), digitalis glycosides , (p.903), and calcium-channel blockers , (p.860). Some antiarrhythmics that do not fit into the Vaughan Williams classification (see Table 9.1 , (below)) are also included in this section (e.g. adenosine). Interactions in which the an-tiarrhythmic drug is the affecting substance, rather than the drug whose activity is altered, are dealt with elsewhere. [Pg.243]

Hypotension, bradycardia, ventricular fibrillation and asystole have been seen in a few patients given amiodarone with propranolol, metoprolol or sotalol (for sotalol, see also Drugs that prolong the QT interval + Other drugs that prolong the QT interval , p.2S7). However, analysis of clinical trials su ests that the combination can be beneficial. Amiodarone may inhibit the metabolism of beta blockers metabolised by CYP2D6, such as metoprolol, which might be a factor in the interaction. [Pg.246]

Ibutilide can prolong the QT interval, therefore caution has been advised about the concurrent use of other drugs that can do the same. Ibutilide is reported not to interact with beta blockers or di-go xin. [Pg.262]

Drug interactions barbiturates, tranquilizers, other narcotics, antihistamines, antidepressants, MAO inhibitors, and alcohol can all increase CNS depression. The risk of bradycardia and hypotension increases for patients on beta blockers and calcium channel blockers. Cimetidine, used to treat peptic ulcers, interacts with sufentanil and increases the risk of respiratory depression. [Pg.193]

Drug interactions occur with many commonly prescribed medications and are mostly due to naproxen s effects on renal prostaglandins and the associated changes in kidney filtration rate, although many other mechanisms exist. Many drug interactions exist, with examples being ACE inhibitors, beta blockers, methotrexate, lithium, probenecid, antiplatelet agents, diuretics, and vancomycin. [Pg.224]


See other pages where Beta blockers interaction with other drugs is mentioned: [Pg.618]    [Pg.243]    [Pg.2573]    [Pg.535]    [Pg.247]    [Pg.847]    [Pg.19]    [Pg.655]    [Pg.338]    [Pg.236]    [Pg.220]    [Pg.779]    [Pg.466]    [Pg.1497]    [Pg.49]    [Pg.146]    [Pg.30]    [Pg.232]    [Pg.841]    [Pg.854]    [Pg.900]    [Pg.944]   
See also in sourсe #XX -- [ Pg.209 , Pg.212 ]




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Beta Interactions

Drug interactions with

Drugs beta-blockers

Interaction with other drugs

Interactions with other

OTHER DRUGS

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