2-amino-N-[2-(2,5-dimethoxyphenyl)-2-hydroxy-ethyl]-acetamide

本品藉著增加已鬆弛血管的張力和預防血液大量滯留於下肢靜脈來升高血壓。

循環失調：成人及青年(12歲以上)：每次一錠，一天2次(早、晚各一錠)。

尿失禁：成人：一次1-2錠，一天2-3錠。

Absorption
Midodrine is rapidly absorbed. Absolute bioavailability is 93%, prodrug T max is 30 min, and metabolite T max is 1 to 2 h.

Distribution
Neither prodrug nor metabolite is bound to plasma proteins to any significant extent.

Metabolism
Major active metabolite is desglymidodrine. Declycination of midodrine to desglymidodrine takes place in many tissues. Both compounds are metabolized in part by the liver.

Elimination
Renal Cl of desglymidodrine is 385 mL/min (approximately 80% by active renal secretion). The t ½ is 25 min (midodrine) and 3 to 4 h (desglymidodrine).

Peak
Time to peak is 1 h.

Duration
Duration is 2 to 3 h.

Special Populations
Renal Function Impairment

Use cautiously in patients with urinary retention problems. A lower starting dose (2.5 mg) may be necessary. Assess renal function prior to initial use.

Hepatic Function Impairment

Use with caution, as the liver has a role in the metabolism.

Alpha-blocking agents (eg, prazosin, terazosin, doxazosin)
May antagonize pressor effects of midodrine.

Cardiac glycosides (ie, digitalis), beta-blockers
May precipitate bradycardia, AV block, or arrhythmia.

Fludrocortisone
May exacerbate supine hypertension.

Vasoconstrictors (eg, dihydroergotamine, ephedrine, phenylephrine, phenylpropanolamine, pseudoephedrine)
May enhance pressor effects of midodrine.