(Generic versions may still be available.)
The primary action of beta-adrenergic drugs, including albuterol, is to stimulate adenyl cyclase, the enzyme which catalyzes the formation of cyclic-3´,5´-adenosine monophosphate (cyclic AMP) from adenosine triphosphate (ATP) in beta-adrenergic cells. The cyclic AMP thus formed mediates the cellular responses. Increased cyclic AMP levels are associated with relaxation of bronchial smooth muscle and inhibition of release of mediators of immediate hypersensitivity from cells, especially from mast cells.
In vitro studies and in vivo pharmacologic studies have demonstrated that albuterol has a preferential effect on beta2-adrenergic receptors compared with isoproterenol. While it is recognized that beta2-adrenergic receptors are the predominant receptors in bronchial smooth muscle, data indicate that there is a population of beta2-receptors in the human heart existing in a concentration between 10% and 50%. The precise function of these receptors has not been established.
In controlled clinical trials, albuterol has been shown to have more effect on the respiratory tract, in the form of bronchial smooth muscle relaxation, than isoproterenol at comparable doses, while producing fewer cardiovascular effects. Controlled clinical studies and other clinical experience have shown that inhaled albuterol, like other beta-adrenergic agonist drugs, can produce a significant cardiovascular effect in some patients, as measured by pulse rate, blood pressure, symptoms, and/or ECG changes.
Albuterol is longer acting than isoproterenol in most patients by any route of administration because it is not a substrate for the cellular uptake processes for catecholamines nor for catechol-O-methyl transferase.
Intravenous studies in rats with albuterol sulfate have demonstrated that albuterol crosses the blood-brain barrier and reaches brain concentrations that are amounting to approximately 5.0% of the plasma concentrations. In structures outside the blood-brain barrier (pineal and pituitary glands), albuterol concentrations were found to be 100 times those in the whole brain.
Studies in laboratory animals (minipigs, rodents, and dogs) have demonstrated the occurrence of cardiac arrhythmias and sudden death (with histologic evidence of myocardial necrosis) when beta-agonists and methylxanthines are administered concurrently. The clinical significance of these findings is unknown.
Albuterol is rapidly and well absorbed following oral administration. After oral administration of 10 mL of VENTOLIN Syrup (albuterol sulfate syrup) (4 mg albuterol) in normal volunteers, maximum plasma albuterol concentrations of about 18 ng/mL are achieved within 2 hours, and the drug is eliminated with a half-life of about 5 to 6 hours.
In other studies, the analysis of urine samples of patients given 8 mg of tritiated albuterol orally showed that 76% of the dose was excreted over 3 days, with the majority of the dose being excreted within the first 24 hours. Sixty percent of this radioactivity was shown to be the metabolite. Feces collected over this period contained 4% of the administered dose.
In controlled clinical trials in patients with asthma, the onset of improvement in pulmonary function, as measured by maximal midexpiratory flow rate (MMEF) and forced expiratory volume in 1 second (FEV1), was within 30 minutes after a dose of VENTOLIN Syrup (albuterol sulfate syrup) . Peak improvement of pulmonary function occurred between 2 and 3 hours. In a controlled clinical trial involving 55 children, clinically significant improvement (defined as maintenance of mean values over baseline of 15% or 20% or more in the FEV1 and MMEF, respectively) continued to be recorded up to 6 hours. No decrease in the effectiveness was reported in one uncontrolled study of 32 children who took VENTOLIN Syrup (albuterol sulfate syrup) for a 3-month period.
Last reviewed on RxList: 12/17/2004
This monograph has been modified to include the generic and brand name in many instances.
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