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17 recordsLinked to original sources
PubMed1976

Pharmacodynamic actions of midodrine, a new alpha-adrenergic stimulating agent, and its main metabolite, ST 1059.

Pharmacodynamic actions of alpha-(2,5-dimethoxyphenyl)-beta-glycinamido-ethanol-hydrochloride (midodrine, Gutron) and alpha-(2,5-dimethoxy-phenyl)-beta-aminoethanol (ST 1059), the main metabolite of midodrine, were investigated in various experimental procedures. Midodrine raises arterial blood pressure both after parenteral and enteral administration in animal experiments. Midodrine increases peripheral vascular tone when given in doses still ineffective in raising blood pressure. The d(+)-isomer of midodrine is by far less effective than the racemic mixture. Pretreatment with atropine, reserpine, guanethidine or hexamethonium has no influence on midodrine activity. Midodrine effects are greatly reduced by phentolamine but rather enhanced by propranolol pretreatment. Midodrine raises blood pressure in pithed rats, too; in the experiments performed the drug is devoid of central effects even when high doses are given. Chronic pretreatment with midodrine over a longer period reduces the effect of a subsequent single injection of this substance. Because of the results cited above midodrine may be classified as a direct peripheral alpha-adrenergic stimulating agent. alpha-Adrenergic receptor stimulation induced by midodrine can be demonstrated in various smooth muscle organs (blood vessels, nictitating membrane, intestine, pupil, urinary bladder, bronchi). In contrast to other pressor sympathomimetic agents, midodrine is of long duration of action and good efficacy after enteral administration. ST 1059, the main metabolite of midodrine, is an active alpha-adrenergic stimulating agent with a shorter duration of action than midodrine. It is suggested that midodrine is the well-absorbed "transport form", from which ST 1059, the actural pressor agent, is formed enzymatically in organism.

Adrenergic alpha-Agonists↗
PubMed2025

Real-World Experience of Midodrine in Hospital Setting in Pulmonary Arterial Hypertension.

BACKGROUND: Pulmonary arterial hypertension (PAH), a progressive disease, is characterized by increased pulmonary vascular resistance (PVR) and leads to right ventricular failure and premature death. PAH therapies aim to reduce PVR; however, these treatments as vasodilators may also result in reduced systemic vascular resistance and mean arterial pressure (MAP), leading to clinical or symptomatic hypotension. Low MAP can limit the administration of optimal dosage of PAH drugs. Midodrine, an oral alpha-1 adrenergic agonist, as a promising intervention, can potentially increase mean MAP and improve tolerance to PAH therapies. RESEARCH QUESTION: Does the use of midodrine improve MAP and allow for simultaneous uptitration of PAH therapy while hospitalized? STUDY DESIGN AND METHODS: A retrospective analysis of 433 patients treated at Houston Methodist Lung Center was undertaken between January 2005 and September 2022. Of these, 57 patients were prescribed midodrine during their hospital stay. We matched 57 patients 1:1 with propensity score matching between patients with PAH not given midodrine (control patients) based on age, sex, World Health Organization functional class, B-type natriuretic peptide, and 6-minute walk distance. RESULTS: Among hospitalized patients with PAH, those receiving midodrine were more likely to undergo uptitration of their PAH medications compared with those not receiving midodrine (n = 30 vs n = 17, respectively; P < .05). Patients on midodrine during hospitalization received higher doses of epoprostenol (P < .001), treprostinil (P < .05), and selexipag (P < .05). Additionally, no adverse effects attributable to midodrine were reported. INTERPRETATION: This study, to our knowledge the first large-scale analysis of PAH data, investigated the use of midodrine in hospitalized patients with PAH. In this single-center study, we share real-world experience of using midodrine to mitigate systemic hypotension, thereby facilitating the uptitration of PAH-targeted therapies.

B-type natriuretic peptide (BNP)↗
PubMed1977

[Investigations of the effect of midodrine on carbohydrate and fat metabolism with particular reference to the diabetic metabolic state (author's transl)].

Midodrine, which is used in the treatment of hypotensive circulatory distrubances was investigated with respect to possible effects on carbohydrate and fat metabolism in 5 healthy subjects and 7 patients with disturbed glocuse tolerance. An i.v. glucose tolerance test was carried out on both groups and was repeated a few days subsequently with simultaneous administration of midodrine (5mg i.v.). Midodrine had no significant effect on glucose tolerance in either group, nor was there any significant effect of midodrine on FFA, serum insulin, triglyceride or cholesterol levels. 15 diabetic patients controlled by different therapeutic regimens (5 by diet only, 5 by oral preparations and 5 by insulin treatment) were given 3x5mg midodrine orally over a 5-day period and the effects on diabetic control and metabolic parameters compared with a 5-day pretreatment period without midodrine. Midodrine did not cause any change in the quality of diabetic control nor any significant alteration in serum lipid or uric acid levels.

Adolescent↗
PubMed1976

Effects of midodrine, ST 1059, methoxamine and glycine on spontaneously beating guinea-pig atria.

The chronotropic effects of midodrine, glycine (10(-8) to 3.10(-3) M), ST1059 and methoxamine (10(-8) to 10(-3) M) were investigated in the spontaneously beating guinea-pig right atrial preparation. Midodrine and glycine produced a slight, but significant rise in atrial rate over a wide concentration range. The midodrine-induced rise in atrial rate was not influenced by the beta-adrenergic receptor blocking drug propranolol (10(-6) M). The histamine (H2)-receptor blocking drug metiamide (3.10(-5) M) abolished the positive chronotropic actions of both midodrine and glycine. No positive chronotropic effect was seen after the administration of ST 1059 or methoxamine. A decrease in atrial rate was elicited by high concentrations (above 10(-4) to 10(-3) M) of the sympathomimetic agents midodrine, ST 1059, and methoxamine, but not by the amino acid glycine.

Adrenergic alpha-Agonists↗
PubMed1979

Plasma level of the prodrug midodrine and its active metabolite in comparison with the alpha-mimetic action in dogs.

Midodrine, i.v. or orally administered, causes a prolonged elevation of blood pressure and a reduction in heart rate. These cardiovascular changes are not correlated to the plasma levels of the intact drug. On administration of either midodrine or its metabolite, ST-1059, formed by cleavage of the glycine residue, the elevation of blood pressure and the reduction in heart rate were significantly correlated to the plasma level of ST-1059. The results are in agreement with the assumption that the pressor activity of midodrine is mainly exerted by its metabolite ST-1059.

Adrenergic alpha-Agonists↗
PubMed1977

Treatment of female stress incontinence with midodrine: preliminary report.

For 10 days 21 female patients with clinical stages I to III stress incontinence and 4 continent control female patients were treated with the alpha-sympathomimetic midodrine. Urethrometry revealed that alpha-adrenergic stimulation resulted in an increase in the urethral occlusion pressure of up to 30 per cent and, cystometrically, to an increase in the detrusor pressure of up to 35 per cent without impairment of bladder capacity. In the stage I group 83 per cent and in the stage II group 63 per cent of the patients became continent. Midodrine, the advantage of which over comparable sympathomimetics, such as ephedrine, synephrine and norphenylephrine, lies in the absolutely sure and sustained action in oral use, is recommended as an alternative therapy to traditional surgical procedures in the treatment of stages I and II female stress incontinence.

Adrenergic alpha-Agonists↗
PubMed1979

The use of Midodrin in the treatment of ejaculation disorders following retroperitoneal lymphadenectomy.

The long-term treatment of retrograde ejaculation disorders following retroperitoneal lymphadenectomy with the alpha-sympathomimetic, Midodrin, administered orally, led to improvements in the intensity of orgasm and the degree of erection. Normal ejaculation was induced in 7 out of 12 patients and emission of spermatozoa into the posterior urethra was restored in 3 out of 12 patients by a single intravenous injection of 25--30 mg Midodrin.

Adult↗
PubMed1979

[Infectious toxic hypotension--effect and dosage of midodrine (author's transl)].

A new alpha-sympathicomimetic drug with peroral effect is midodrine. The effective oral dosage in infancy and childhood is 0.06 mg/kg/dosi. The therapeutic effect, comparing the drug with etilefrin is shown in 120 children with pneumonia, enteritis, meningitis in a random study. The results give an increase in blood pressure and a decrease in heart frequency, statistically proved, on the first day of treatment. Therefore it seems that midodrine is qualified for the treatment of hypotension in infectious diseases.

Bacterial Infections↗
PubMed1978

Assessment of pharmacological effects on cerebral blood flow.

The effect of various drugs on hemispheric and regional cerebral blood flow (CBF) was investigated in a total of 410 patients. While a few drugs (midodrin, proxazole, vincamine, hexobendine, extract of ginkgo biloba, dextran and ouabain) were able to improve hemispheric CBF, only ephedrine combined with xanthines decreased CBF. For vincamine the dependency of the effect on certain plasma levels was established. Only ouabain of the tested cardiac glycosides effected CBF; their similar hemodynamic actions suggest here an influence of ouabain on cerebral vessels. For the evaluation of drug effects on rCBF the detection of heterogeneous responses is important. Such responses may be quantified by regression analysis. While intracerebral steal effects were observed only under certain circumstances, inverse cerebral steal phenomena may be caused by diverging actions of several drugs. If treatment is aimed at improvement of cerebral hemodynamics, only drugs with a demonstrated effect, at least on perfusion of ischemic regions, should be employed.

Cerebrovascular Circulation↗
PubMed1979

[Diagnosis and therapy of hypotensive circulatory disorders in general practice. Experiences with Gutron using the Thulesius-diagram for diagnosis and supervision of therapy].

The alpha-adrenergic stimulating agent Gutron, given orally for 10 days, induced a subjective and objective improvement of orthostatic disorders in a total of 114 hypotensive patients in 7 general practices. The use of the Thulesius diagram in diagnosing orthostatic disorders further improved the rate of success and diminished the frequency of side effects distinctly. Gutron is indicated in all patients with a systolic blood pressure fall of at least 10 mmHg and a concomitant rise in heart rate when changing from lying to standing position (asympathicotonic and sympathicotonic hypotension).

Adult↗