گروه درمانی
داروهای اتونومیک
داروهای مقلد سمپاتیک(آدرنرژیک ها)
داروهای آگونیست آلفا آدرنرژیک
اطلاعات دارو
موارد مصرف میدودرین
Vasopressor/Antihypotensive
Midodrine hydrochloride tablets are indicated for the treatment of symptomatic orthostatic hypotension (OH). Because Midodrine HCl can cause marked elevation of supine blood pressure (BP >200 mmHg systolic), it should be used in patients whose lives are considerably impaired despite standard clinical care, including non-pharmacologic treatment (such as support stockings), fluid expansion, and lifestyle alterations. The indication is based on Midodrine HCl's effect on increases in 1-minute standing systolic blood pressure, a surrogate marker considered likely to correspond to a clinical benefit. At present, however, clinical benefits of Midodrine HCl, principally improved ability to perform life activities, have not been established. Further clinical trials are underway to verify and describe the clinical benefits of Midodrine HCl.
Midodrine hydrochloride tablets are indicated for the treatment of symptomatic orthostatic hypotension (OH). Because Midodrine HCl can cause marked elevation of supine blood pressure (BP >200 mmHg systolic), it should be used in patients whose lives are considerably impaired despite standard clinical care, including non-pharmacologic treatment (such as support stockings), fluid expansion, and lifestyle alterations. The indication is based on Midodrine HCl's effect on increases in 1-minute standing systolic blood pressure, a surrogate marker considered likely to correspond to a clinical benefit. At present, however, clinical benefits of Midodrine HCl, principally improved ability to perform life activities, have not been established. Further clinical trials are underway to verify and describe the clinical benefits of Midodrine HCl.
مکانیسم اثر میدودرین
Midodrine hydrochloride forms an active metabolite, desglyMidodrine, that is an alpha1-agonist, and exerts its actions via activation of the alpha-adrenergic receptors of the arteriolar and venous vasculature, producing an increase in vascular tone and elevation of blood pressure. DesglyMidodrine does not stimulate cardiac beta-adrenergic receptors. DesglyMidodrine diffuses poorly across the blood-brain barrier, and is therefore not associated with effects on the central nervous system. Administration of Midodrine HCl results in a rise in standing, sitting, and supine systolic and diastolic blood pressure in patients with orthostatic hypotension of various etiologies. Standing systolic blood pressure is elevated by approximately 15 to 30 mmHg at 1 hour after a 10 mg dose of Midodrine, with some effect persisting for 2 to 3 hours. Midodrine HCl has no clinically significant effect on standing or supine pulse rates in patients with autonomic failure.
فارماکوکینتیک میدودرین
Midodrine HCl is a prodrug, i.e., the therapeutic effect of orally administered Midodrine is due to the major metabolite desglyMidodrine, formed by deglycination of Midodrine. After oral administration, Midodrine HCl is rapidly absorbed. The plasma levels of the prodrug peak after about half an hour, and decline with a half-life of approximately 25 minutes, while the metabolite reaches peak blood concentrations about 1 to 2 hours after a dose of Midodrine and has a half-life of about 3 to 4 hours. The absolute bioavailability of Midodrine (measured as desglyMidodrine) is 93%. The bioavailability of desglyMidodrine is not affected by food. Approximately the same amount of desglyMidodrine is formed after intravenous and oral administration of Midodrine. Neither Midodrine nor desglyMidodrine is bound to plasma proteins to any significant extent.