Co-administration of such drugs with propranolol may lead to clinically relevant drug interactions and changes on its efficacy and/or toxicity (see Quinidine increases the concentration of propranolol and produces greater degrees of clinical beta-blockade and may cause postural hypotension.Amiodarone is an antiarrhythmic agent with negative chronotropic properties that may be additive to those seen with β-blockers such as propranolol.The clearance of lidocaine is reduced with administration of propranolol. Peak plasma concentrations occur about 1 to 4 hours after an oral dose.Administration of protein-rich foods increase the bioavailability of propranolol by about 50% with no change in time to peak concentration, plasma binding, half-life, or the amount of unchanged drug in the urine.Approximately 90% of circulating propranolol is bound to plasma proteins (albumin and alphaPropranolol crosses the blood-brain barrier and the placenta, and is distributed into breast milk.Propranolol is extensively metabolized with most metabolites appearing in the urine. Propranolol hydrochloride is not indicated for the treatment of tremor associated with Parkinsonism.Propranolol hydrochloride improves NYHA functional class in symptomatic patients with hypertrophic subaortic stenosis.Propranolol hydrochloride is indicated as an adjunct to alpha-adrenergic blockade to control blood pressure and reduce symptoms of catecholamine-secreting tumors.Propranolol hydrochloride is contraindicated in: 1) cardiogenic shock; 2) sinus bradycardia and greater than first degree block; 3) bronchial asthma; and 4) in patients with known hypersensitivity to propranolol hydrochloride.Hypersensitivity reactions, including anaphylactic/anaphylactoid reactions, have been associated with the administration of propranolol (see Cutaneous reactions, including Stevens-Johnson Syndrome, toxic epidermal necrolysis, exfoliative dermatitis, erythema multiforme, and urticaria, have been reported with use of propranolol (see Sympathetic stimulation may be a vital component supporting circulatory function in patients with congestive heart failure, and its inhibition by beta-blockade may precipitate more severe failure. Artemether. or q.i.d. Interactions with Substrates, Inhibitors or Inducers of Cytochrome P-450 Enzymes:There have been reports of exacerbation of angina and, in some cases, myocardial infarction, following abrupt discontinuance of propranolol therapy. Severe Interactions.
Such patients may be unresponsive to the usual doses of epinephrine used to treat allergic reaction.In patients with hypertension, use of propranolol has been associated with elevated levels of serum potassium, serum transaminases and alkaline phosphatase. Beta-adrenergic receptors have been demonstrated in the pial vessels of the brain.The specific mechanism of propranolol’s antitremor effects has not been established, but beta-2 (noncardiac) receptors may be involved. It specifically competes with beta-adrenergic receptor agonist agents for available receptor sites. Propranolol should be administered with caution in this setting since it may provoke a bronchial asthmatic attack by blocking bronchodilation produced by endogenous and exogenous catecholamine stimulation of beta-receptors.Chronically administered beta-blocking therapy should not be routinely withdrawn prior to major surgery, however the impaired ability of the heart to respond to reflex adrenergic stimuli may augment the risks of general anesthesia and surgical procedures.Beta-adrenergic blockade may prevent the appearance of certain premonitory signs and symptoms (pulse rate and pressure changes) of acute hypoglycemia, especially in labile insulin-dependent diabetics.