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PubMed1986

Effects of midodrine on blood flow in dog vascular beds.

Effects of alpha-(2,5-dimethoxyphenyl)-beta-glycinamide-ethanol hydrochloride (midodrine, ST-1085) on blood flow in different vascular beds were examined in anesthetized dogs. Intravenously administered midodrine at doses of 0.3 and 0.6 mg/kg induced a transient increase followed by a long-lasting decrease in femoral arterial blood flow. Renal arterial blood flow exhibited an initial decrease followed by returning toward the control level, and thereafter decreased again. Vertebral, common carotid, superior mesenteric and coronary arterial blood flow, and cardiac output gradually decreased. Midodrine did not have any effects on cerebral tissue blood flow. The changes were more remarkable at a dose of 0.6 mg/kg than at 0.3 mg/kg. Each arterial blood flow change was statistically analyzed 20, 30 and 60 min after the administration of 0.6 mg/kg of midodrine. The decrease of coronary arterial blood flow by the treatment with midodrine was significantly smaller than those of superior mesenteric and femoral arterial blood flow at 20 and 30 min after midodrine administration. The decrease of renal arterial blood flow was significantly smaller than those of superior mesenteric arterial blood flow at 20 and 30 min, and femoral arterial blood flow at 20, 30 and 60 min after the administration. The decrease of vertebral arterial blood flow was also smaller than that of femoral arterial blood flow at 20, 30 and 60 min after the administration.

Adrenergic alpha-Agonists↗
PubMed1980

Central action of intraventricularly-injected midodrine in rats.

The aim of the present paper was to investigate the effect of intracerebroventricular (i.v.c.) injections of midodrine on the central nervous system of the rat. It was shown that midodrine increased locomotor activity, decreased body temperature, increased sedation in reserpinized rats and the cataleptic effect of haloperidol. Midodrine enhanced amphetamine-stimulated locomotor activity and reduced the amphetamine and apomorphine sterotypy. Phenoxybenzamine, yohimbine and clonidine inhibited the midodrine-induced hyperactivity. Midodrine depressed the whole brain noradrenaline (NA) and dopamine (DA) concentrations and reduced NA turnover. The results suggest a stimulating action of midodrine on the catecholaminergic neurons.

Animals↗
PubMed1998

Acute effects of the oral administration of midodrine, an alpha-adrenergic agonist, on renal hemodynamics and renal function in cirrhotic patients with ascites.

The effects of the acute administration of arterial vasoconstrictors on renal plasma flow (RPF) and urinary sodium excretion (UNaV) in cirrhotic patients with ascites with or without hepatorenal syndrome (HRS) are still controversial. As a consequence, vasoconstrictors are not actually used in the treatment of renal sodium retention or HRS in these patients, regardless of the several lines of evidence suggesting that these renal functional abnormalities are related to a marked arterial vasodilation. The lack of an orally available effective arterial vasoconstrictor probably represents a further reason for this omission. Consequently, the present study was made to evaluate the acute effects of the oral administration of midodrine, an orally available -mimetic drug, on systemic and renal hemodynamics and on UNaV in cirrhotic patients with ascites. Mean arterial pressure (MAP), heart rate (HR), cardiac index (CI), systemic vascular resistance (SVR), left forearm blood flow (LFBF), left leg blood flow (LLBF), RPF, glomerular filtration rate (GFR), UNaV, plasma renin activity (PRA), plasma concentration of antidiuretic hormone (ADH), and the serum levels of nitrite and nitrate (NOx) were evaluated in 25 cirrhotic patients with ascites (17 without HRS and 8 with type 2 HRS) before and during the 6 hours following the oral administration of 15 mg of midodrine. During the first 3 hours after the drug administration, a significant increase in MAP (89.6 +/- 1.7 vs. 81.80 +/- 1.3 mm Hg; P < .0001) and SVR (1, 313.9 +/- 44.4 vs. 1,121.2 +/- 60.1 dyn . sec . cm-5; P < .0001) accompanied by a decrease in HR (69 +/- 2 vs. 77 +/- 3 bpm; P < .005) and CI (2,932.7 +/- 131.4 vs. 3,152.5 +/- 131.4 mL . min-1 . m2 BSA; P < .0025) was observed in patients without HRS. No change was observed in LFBF and LLBF. The improvement in systemic hemodynamics, which was also maintained during the the 3- to 6-hour period after midodrine administration, was accompanied by a significant increase in RPF (541.5 +/- 43.1 vs. 385.7 +/- 39.9 mL . min-1; P < .005), GFR (93.1 +/- 6.5 vs. 77.0 +/- 6.7 mL . min-1; P < .025), and UNaV (92.7 +/- 16.4 vs. 72.2 +/- 10.7 microEq . min-1; P < .025). In addition, a decrease in PRA (5.33 +/- 1.47 vs. 7.74 +/- 2.17 ng . mL-1 . h; P < .05), ADH (1.4 +/- 0.2 vs. 1.7 +/- 0.2 pg . mL-1; P < .05), and NOx (33.4 +/- 5.0 vs. 49.3 +/- 7.3 micromol-1; P < .05) was found. In patients with HRS, the effects of the drug on the systemic hemodynamics was smaller and shorter. Accordingly, regardless of a significant decrease in PRA (15.87 +/- 3.70 vs. 20.70 +/- 4.82 ng . mL-1 . h; P < .0025) in patients with HRS, no significant improvement was observed in RPF, GFR, or UNaV. In conclusion, the acute oral administration of midodrine is associated with a significant improvement in systemic hemodynamics in nonazotemic cirrhotic patients with ascites. As a result, renal perfusion and UNaV also improve in these patients. By contrast, midodrine only slightly improves systemic hemodynamics in patients with type 2 HRS, with no effect on renal hemodynamics and renal function.

Administration, Oral↗
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↗
PubMed1995

Preliminary observations on the use of midodrine in treating orthostatic hypotension in familial dysautonomia.

Midodrine, a peripheral alpha-adrenergic agonist, was evaluated in 7 female and 2 male patients with familial dysautonomia (FD), a disorder characterized by decreased sympathetic innervation. Prior to and after three months of midodrine treatment, each patient's response to postural change was assessed by arteriosonde readings of blood pressure and heart rate, corrected QT-interval measurements, Doppler evaluation of renal blood flow and circulating atrial natriuretic peptide (ANP) levels. The initial midodrine dose (2.5 mg three times daily) was raised until subjective symptoms improved. Doses were reduced if patients felt jittery or developed erect hypertension (systolic > 180 mmHg or diastolic > 110 mmHg). Midodrine, at an average dose of 0.25 mg/kg per day, improved subjective symptoms in all patients. With treatment, magnitude of blood pressure responses was variable. Although mean erect blood pressure did not increase significantly for the aggregate, it did increase in six of nine patients. In addition, the QTc interval normalized and erect renal perfusion improved. Changes in supine mean blood pressure and supine circulating ANP correlated directly. We judge midodrine to be useful in management of orthostatic hypotension in patients with familial dysautonomia.

Adolescent↗
PubMed2005

[Treatment of ejaculation disorders by midodrine (Gutron) per os. Retrospective study of about 16 subjects].

PURPOSE: We evaluate the efficiency and side effects of midodrine in the treatment of sperm transport disturbances. MATERIALS AND METHODS: This retrospective study concerned patients addressed in Andrologia Department between 1995 and 2002 for treatment of sperm transport disturbances by administration of Midodrine per os (from 2.5 to 20 mg). Anterograde and retrogrades ejaculates (in urine sample) were examined. RESULTS: Sixteen patients (middle age of 36 years) were included: 12 neurologic lesions (central or peripheral, with 3 diabetes), four post-surgical (urologic and digestive) ejaculatory incompetence. One patient obtained anterior and retrograde ejaculation, two patients obtained anterior ejaculation and six retrograde ejaculations by midodrine per os. This treatment was inefficient in eight subjects. Side effects were exceptional. DISCUSSION: We obtained anterior or retrograde ejaculation in half of our population. The success was more important in patients with central neurologic injuries, diabetes or post-surgical troubles. In peripheral neurologic injuries, midodrine per os (maximal dose of 20 mg) was ineffective. CONCLUSION: Our study demonstrates the efficiency and good tolerance of midodrine per os for treatment of sperm transport disturbances.

Adrenergic alpha-Agonists↗
PubMed2002

Hemodynamics in patients with intradialytic hypotension treated with cool dialysate or midodrine.

Cool dialysate and midodrine have been used successfully to treat intradialytic hypotension (IDH) in the end-stage renal disease population. However, the exact mechanisms by which these interventions improve hemodynamic stability are not well known. We undertook a study to evaluate the effect of these modalities on intradialytic hemodynamics in patients with documented dialysis-associated hypotension. We used the ultrasound dilution technique to measure cardiac output (CO), central blood volume (CBV), and peripheral vascular resistance (PVR) in these patients. The study was performed in two phases. Phase 1 consisted of control (1A) and cool dialysate (1B) studies, whereas phase 2 consisted of control (2A) and midodrine (2B) studies. CO, CBV, and PVR were measured 30 minutes after the initiation of hemodialysis (HD) and 30 minutes before the termination of HD using the HD01 monitor. Blood pressure was measured pre-HD and post-HD. Fourteen patients with documented IDH completed the study. CO and CBV were significantly more preserved in the cool dialysate and midodrine phases compared with control phases. PVR increased in all phases of the study. Declines in mean arterial pressures from pre-HD to post-HD were less with cool dialysate versus control and midodrine versus control. Ultrafiltration volumes were not significantly different between phases. Cool dialysate and midodrine appear to improve intradialytic hemodynamics in patients with dialysis-associated hypotension, mainly through the preservation of CBV and CO, rather than significantly elevating PVR.

Adrenergic alpha-Agonists↗
PubMed2004

Double-blinded, placebo-controlled trial of midodrine for exercise performance enhancement in tetraplegia: a pilot study.

BACKGROUND/OBJECTIVE: Spinal cord injury (SCI) impairs cardiovascular autonomic responses to exercise and, depending on the level of injury, may result in hypotension and pathologic fatigue with exertion. Other clinical populations with sympathetic regulatory dysfunction, but without skeletal muscle paralysis, exhibit similar signs and symptoms. Their ability to engage in physical activity improves with elevation of blood pressure through pharmacologic treatment: Midodrine, an oral alpha-sympathomimetic agent, has been shown to be safe and efficacious for this purpose. Use of this medication in individuals with SCI merits investigation. METHODS: Double-blind, placebo-controlled, randomized, crossover, within-subjects protocol. Four participants with chronic, motor-complete injuries from C6 to C8 underwent 4 peak exercise tests (PXT) using a wheelchair ergometer, following administration of midodrine, 5 mg, 10 mg, and placebo, in random order. Heart rate, blood pressure, oxygen consumption (VO2), and perceived exertion were measured. RESULTS: Treatment with midodrine, 10 mg, was associated with elevated systolic blood pressure during peak exercise in 3 participants. Two participants showed a concurrent decrease in perceived exertion and increase in VO2. No adverse effects of midodrine were evident. CONCLUSION: Midodrine enhances exercise performance in some individuals with SCI, similar to other clinical populations with cardiovascular autonomic dysfunction.

Adrenergic alpha-Agonists↗
PubMed2004

[Results of midodrin treatment of vasovagal syncope].

AIM: To elicit efficacy of midodrin in patients with vasovagal syncope. MATERIAL AND METHODS: 50 patients with recurrent vasovagal syncope documented by head-up tilt tests or bicycle exercise stress tests participated in the study. These tests controlled the effects of midodrin if syncopes occurred again in repetition of the tests. In the other patients the effect of the drug was assessed clinically. All the patients received midodrin in daily dose up to 15 mg. RESULTS: Mirodrin effectively prevented syncope in 13 (72%) patients as shown by the tilt test, in 10 (59%) patients as shown by the exercise stress tests and in 14 (93%) patients as controlled clinically. Total efficacy of midodrin was 74% (37 of 50 patients). CONCLUSION: Midodrin demonstrated high efficacy in prevention of vasovagal syncope. Side effects were not serious therefore the drug is well tolerated.

Adolescent↗
PubMed1987

[The bioavailability of midodrin and alpha-2,5-dimethoxyphenyl-beta-aminoethanol hydrochloride].

The pharmacokinetics of midodrin (alpha-2,5-dimethoxyphenyl-beta-glycinamidoethanol hydrochloride, ST 1085) and its main metabolite ST 1059 (alpha-2,5-dimethoxyphenyl-beta-aminoethanol hydrochloride) have been investigated in 12 male healthy volunteers. 2.5 mg midodrin hydrochloride were applied intravenously, as drinking solution or as tablet (Gutron) according to a randomized cross-over design. Plasma and urine samples collected up to 24 h after application were analyzed by high-performance liquid chromatography with fluorescence detection. The mean maximum concentration in plasma for midodrin was ca. 10 ng/ml 20-30 min after oral administration, for ST 1059 ca. 5 ng/ml after 1 h. Midodrin was eliminated with a terminal half-life of 0.5 h. The half-life of ST 1059 was determined to be 3 h. The mean area under the plasma-level vs. time curve (AUC) of ST 1059 after administration of 2.5 mg midodrin i.v. was 28.7 ng X h/ml, and as drinking solution or as tablet 25.7 and 25.6 ng X h/ml, respectively. The data of 10 volunteers could be used for the calculations of the bioavailability of ST 1059 by the AUC. Assuming an interval of equivalence of 0.75-1.25 because of the relatively small number of volunteers, the three galenical formulations are considered to be equivalent.

Administration, Oral↗
PubMed1987

Effects of midodrine on experimentally induced postural hypotension and venous pooling in dogs.

Effects of (+/-)-2-amino-N-2,5-(dimethoxyphenyl-beta-hydroxyphenyl) acetamide hydrochloride (midodrine) on experimental postural hypotension and venous pooling were examined in the anesthetized dog treated with hexamethonium (20 mg/kg s.c.). A 30 degree-tilt caused a significant decrease in blood pressure. Midodrine, at 0.1 mg/kg, significantly attenuated the decrease in blood pressure induced by the tilt 10, 20 and 30 min after its administration. The heart rate was not affected by the tilt. Cardiac output decreased significantly following the tilt. Midodrine significantly increased the basal rate of cardiac output and attenuated the decrease in cardiac output induced by the tilt. Venous pooling was produced by the occlusion of the circulation of the dog foot, and the increase of limb girth by the cuff inflating was measured as an indicator of venous pooling. Midodrine, at 0.1 mg/kg, significantly attenuated the increase of limb girth, indicating that the drug reduced venous pooling. These results suggest that midodrine (0.1 mg/kg i.v.) constricts the venous bed, resulting in the increase in cardiac output in the anesthetized dog with experimental postural hypotension.

Animals↗
PubMed1999

Reversal of type 1 hepatorenal syndrome with the administration of midodrine and octreotide.

The aim of the study was to verify the effects of the administration of an inhibitor of the release of endogenous vasodilators together with a vasoconstrictor agent in patients with hepatorenal syndrome (HRS). This new medical perspective was compared with a traditional medical approach for HRS, such as the infusion of nonpressor doses of dopamine to produce renal vasodilation. Thirteen patients with type 1 HRS were enrolled in the study. Five of them were treated with the oral administration of midodrine and the parenteral administration of octreotide. In addition, the patients received 50 to 100 mL of 20% human albumin solution daily for 20 days. Midodrine and octreotide were dosed to obtain a stable increase of at least 15 mm Hg of mean arterial pressure. Eight patients were treated with the intravenous administration of nonpressor doses of dopamine (2-4 micrograms/kg/min) and the same daily amount of albumin. After 20 days of treatment with midodrine and octreotide, an impressive improvement in renal plasma flow (RPF), glomerular filtration rate, and urinary sodium excretion was observed in patients. This was accompanied by a significant reduction in plasma renin activity, plasma vasopressin, and plasma glucagon. No side effects were observed. Three patients were discharged from the hospital. One of them successfully underwent liver transplantation. One of the two remaining patients is still alive after 472 days with a preserved renal function, and the other died from terminal liver failure after 76 days. One of the two patients who were not discharged from the hospital successfully underwent liver transplantation, and the other died from pneumonia after 29 days. Seven out of eight patients who were treated with dopamine experienced a progressive deterioration in renal function and died during the first 12 days. Only one patient recovered renal function and underwent liver transplantation. In conclusion, the long-term administration of midodrine and octreotide seems to be an effective and safe treatment of type 1 HRS in patients with cirrhosis.

Aldosterone↗
PubMed1994

A comparison of postspace-flight orthostatic intolerance to vasovagal syncope and autonomic failure and the potential use of the alpha agonist midodrine for these conditions.

After space-flights of less than ten days, orthostatic hypotension upon reentry is characterized by plasma volume depletion that may lead to activation of the Bezold-Jarisch reflex which is also considered to be the mechanism of vasovagal (neurocardiogenic) syncope. For space-flight of longer duration, loss of cardiovascular reflex control may take precedence over volume depletion and thus may have similarities to the orthostatic hypotension seen in patients with autonomic failure secondary to basal ganglial disease and peripheral neuropathies. Midodrine is an alpha-one agonist that produces arterial and venous constriction and leads to a decrease in heart rate by baroreceptor reflexes. The efficacy of Midodrine in successfully treating orthostatic hypotension secondary to autonomic failure has been shown in clinical trials. Midodrine's ability to vasoconstrict without increasing heart rate suggests that it might be a useful treatment for vasovagal syncope since stimulation of the Bezold-Jarisch reflex would be less likely. For post-space flight orthostatic hypotension, midodrine may be a useful adjunctive treatment to the measures currently being used.

Adult↗
PubMed1998

Randomized double-blind placebo-controlled multicenter evaluation of efficacy and dose finding of midodrine hydrochloride in women with mild to moderate stress urinary incontinence: a phase II study.

Midodrine is a potent and selective alpha1-receptor agonist and its potential to increase urethral closure pressure could be useful in the treatment of female stress incontinence. The aim of this randomized double-blind placebo-controlled multicenter study was to evaluate the efficacy and safety of midodrine for the treatment of stress urinary incontinence. The primary criterion of efficacy was the maximum urethral closure pressure at rest. Voiding diaries, symptom and incontinence questionnaires and patient/investigator global assessment were also used to evaluate its efficacy. After 4 weeks of treatment no significant changes in MUCP were found. The global assessment by the patient and investigator did indicate that patients on active treatment had a more positive assessment than the placebo group. In conclusion, midodrine did not cause significant improvements in urodynamic parameters, but there were subjective improvements in some of the patients in the treated groups. Furthermore midodrine was well tolerated.

Adrenergic alpha-Agonists↗
PubMed2006

Effects of a 7-day treatment with midodrine in non-azotemic cirrhotic patients with and without ascites.

BACKGROUND/AIMS: Splanchnic arterial vasodilatation has been causally related with hyperdynamic circulation and impaired natriuresis in advanced cirrhosis and has also been suggested to be responsible for the subtle sodium retention in pre-ascitic cirrhosis. This study evaluated the effects of a 7-day treatment with the alpha1-adrenergic agonist midodrine in non-azotemic cirrhotic patients with and without ascites. METHODS: Thirty-nine cirrhotic patients were studied at baseline and 7 days after administration of oral midodrine 10mg, t.i.d. (11 without and 12 with ascites) or placebo (8 without and 8 with ascites). RESULTS: A significant increase in urine sodium excretion was noted after midodrine administration in patients without and with ascites, in line with significant increases in mean arterial pressure and systemic vascular resistance, and significant decreases in cardiac output and heart rate. Significant increases in glomerular filtration rate, filtration fraction, and urine volume and significant decreases in plasma renin activity and aldosterone were observed in patients with ascites. Placebo had no effect in any study group. CONCLUSIONS: The administration of midodrine for 7 days improves systemic haemodynamics and sodium excretion in non-azotemic cirrhotic patients without or with ascites. In patients with ascites, but not in those without ascites, these effects are associated with a suppression of the activity of the renin-angiotensin-aldosterone system, suggesting that the increase in natriuresis is related to the improvement in the effective arterial blood volume.

Adrenergic alpha-Agonists↗
PubMed2006

The efficacy of midodrine hydrochloride in the treatment of children with vasovagal syncope.

OBJECTIVE: To determine whether midodrine hydrochloride therapy can prevent vasovagal syncope (VVS) in pediatric patients. STUDY DESIGN: Children with recurrent syncope (n = 26) were randomly assigned into 2 groups. Group I comprised children given midodrine hydrochloride as first-line therapy in addition to conventional therapy, and group II comprised patients receiving conventional therapy only. Repeat head-up tilt (HUT) testing and follow-up of least 6 months were conducted to evaluate the therapeutic effectiveness and side effects of midodrine in treating VVS in children. RESULTS: The HUT-based effective rate was significantly higher in group I than in group II (75% vs 20%; P < .05). During the follow-up period, the recurrence of syncope was significantly lower in group I than in group II (P < .05). CONCLUSIONS: Midodrine hydrochlorate is effective in treating VVS in children, especially in preventing recurrent episodes. Few side effects were observed in the present study.

Adolescent↗
PubMed2003

Effects of fatty acids and iontophoresis on the delivery of midodrine hydrochloride and the structure of human skin.

PURPOSE: The purpose of this work was to investigate if fatty acids can increase the iontophoretic delivery of midodrine hydrochloride through human dermatomed skin and to observe the effects of iontophoresis and fatty acids on skin using SEM. METHODS: After prehydration for 1 h, human dermatomed skin was treated with 0-0.3 M fatty acids (oleic acid, linoleic acid, decanoic acid, and lauric acid) in propylene glycol (PG) for 1 h. Then the fatty acid solution was replaced by 1% midodrine hydrochloride aqueous solution, and 0.1 mA/cm2 constant current was applied. Samples were taken over 24 h and analyzed by HPLC. After the treatments outlined above, the epidermis was separated, fixed with glutaraldehyde, and dehydrated for SEM. RESULTS: SEM studies revealed that only 1 h of treatment with fatty acids opened up the tightly compact stratum corneum cell layer, and the permeation study showed a significant increase of the permeability of skin to midodrine hydrochloride after fatty acid treatment. CONCLUSIONS: Using 5% oleic acid pretreatment, with the electrical current offset at 0.1 mA/cm2, the daily delivery of midodrine hydrochloride can provide an adequate clinical application. The enhancement of passive and iontophoretic delivery by fatty acids may be occurring through the same mechanism.

Adjuvants, Pharmaceutic↗
PubMed1988

Treatment of orthostatic hypotension due to autonomic failure with a peripheral alpha-adrenergic agonist (midodrine).

The therapeutic efficacy of midodrine, an alpha-adrenergic agonist that does not cross the blood-brain barrier, was investigated in a double-blind crossover trial in seven patients with orthostatic hypotension due to autonomic failure. We identified two groups of patients: those in whom upright mean arterial pressure significantly increased (group I, n = 3) and those in whom upright mean arterial pressure decreased (group II, n = 4) during midodrine treatment. Body weight changed in a parallel manner with upright blood pressure, increasing in patients of group I and decreasing in patients of group II (p less than 0.05). Autonomic cardiovascular reflexes were significantly more impaired in patients of group II than in patients of group I. We conclude that midodrine is effective in the treatment of orthostatic hypotension only in those patients with significant preservation of autonomic reflexes. Conversely, in patients with markedly impaired baroreceptor mechanisms, treatment with midodrine may produce extracellular fluid volume depletion and exacerbate orthostatic hypotension.

Adrenergic alpha-Agonists↗