Alpha Receptor Agonist Toxicity
| Autor: | Norman K; St. Luke's University Health Network, Nappe TM; St. Luke's University Health Network; Lewis Katz School of Medicine, Temple University |
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| Jazyk: | angličtina |
| Zdroj: | 2022 Jan. |
| Abstrakt: | Alpha-adrenergic agonist toxicity is due to a broad group of pharmaceutical agents known as alpha agonists, which can be further broken down into central alpha-2 agonists and peripheral alpha-1 agonists. Central alpha-2 agonists include clonidine, guanfacine, tizanidine, guanabenz, and methyldopa. Peripheral alpha-1 agonists include imidazoline, oxymetazoline, tetrahydrozoline, and naphazoline. Mainly there are 2 alpha receptors of pharmacological significance – central alpha-2 and peripheral alpha-1 adrenergic receptors. Stimulation of central alpha-2 receptors causes decreased secretion of catecholamines through a negative feedback mechanism. Stimulation of peripheral alpha-1 receptors primarily increases blood pressure via induced vasoconstriction. Alpha-adrenergic agonist toxicity is of primary concern with alpha-2 adrenergic agonist xenobiotics through the resulting depletion of catecholamines associated with these agents; however, there are many topical alpha-1 agonists that when misused cause similar toxicity. Toxicity is encountered in various populations, particularly in children and adolescents, due to the growing use of these agents. Toxicity is associated with a compilation of symptoms, including central nervous system depression, bradycardia, and hypotension. Alpha-adrenergic toxicity is often very responsive to supportive care, including intravenous fluid administration, airway monitoring, and repletion of catecholamines as necessary via the use of vasopressor agents. There is no antidote approved for human use, and naloxone has no proven efficacy. (Copyright © 2022, StatPearls Publishing LLC.) |
| Databáze: | MEDLINE |
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