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PubMed2004

Midodrine appears to be safe and effective for dialysis-induced hypotension: a systematic review.

BACKGROUND: Dialysis-induced hypotension is an important complication of haemodialysis. Midodrine is an oral alpha-1 agonist that has been used in several small studies to prevent intradialytic hypotension (IDH). METHODS: The authors searched MEDLINE, EMBASE, ASN conference proceedings, and references of potentially relevant articles, and contacted industry (Shire Pharmaceuticals) for unpublished data. Observational studies, randomized controlled trials, crossover studies and pre- and post-intervention design studies with >/=5 haemodialysis patients were included. Study outcomes assessed were: hypotensive symptoms, changes in systolic and/or diastolic blood pressure, dry weight and length of stay after treatment. Data were abstracted on: study design, patient characteristics, intradialytic changes in blood pressure, nadir blood pressure and symptom improvement with midodrine. Thirty-seven full text articles were retrieved and nine met the selection criteria, in addition to one unpublished study. Midodrine dosing regimens ranged from 2.5 to 10 mg of midodrine given 15-30 min before dialysis. RESULTS: Post-dialysis systolic blood pressure was higher by 12.4 mmHg [95% confidence interval (CI) 7.5-17.7] and diastolic pressure was higher by 7.3 mmHg (95% CI 3.7-10.9) during midodrine treatment vs control. Likewise, the nadir systolic blood pressure was higher by 13.3 mmHg (95% CI 8.6-18.0), with a difference in nadir diastolic pressure of 5.9 mmHg (95% CI 2.7-9.1). Six of 10 studies report improvement in symptoms of IDH, and there were no reported serious adverse events ascribed to midodrine. CONCLUSIONS: This systematic review would suggest that midodrine has a role in the therapy of haemodialysis patients experiencing IDH. This conclusion must be viewed with caution, however, given the quality and sample size of the studies included in this review.

Adrenergic alpha-Agonists↗
PubMed1998

Treatment of orthostatic hypotension with midodrine and octreotide.

The purpose of this study was to compare two treatments for orthostatic hypotension, midodrine (an alpha adrenergic agonist), and octreotide (an SRIH analogue) to each other and to combination therapy. Sixteen patients participated. Our hypothesis was that the 2 drugs together would be more effective than either drug alone. The effect of the drugs on the hemodynamic response to food ingestion was evaluated while patients were sitting. Midodrine (5 mg orally, 30 min before breakfast) increased mean blood pressure slightly (5-10 mm Hg, over 30 min) before the patients started eating, but it only partially reversed the hypotensive effect of food ingestion. The nadir in postprandial blood pressure after midodrine was 69 +/- 4 mm Hg, not different from placebo (63 +/- 5). Nevertheless, midodrine accentuated the response to sc octreotide (0.5 microgram/kg). Fifteen minutes after octreotide administration to midodrine-pretreated patients, the average mean blood pressure was 115 +/- 9 mm Hg, higher (P = .0095) than after octreotide given alone (102 +/- 7). Drug effects on orthostatic hypotension were assessed by measuring standing time (minutes before symptoms of hypotension or definite hypotension). In the absence of treatment, standing time was 3.5 +/- 7 min; 1 h after 10 mg midodrine, 8.4 +/- 2.7 min (P = .11); after 1.0 microgram/kg octreotide, 13.2 +/- 3.9 min (P = .0034 vs. no treatment); and after both drugs, 21.2 +/- 5.5 min (P = .0002 vs. no treatment, P = .036 vs. octreotide only). The combination of midodrine and octreotide is more potent than either drug alone.

Adrenergic alpha-Agonists↗
PubMed2000

Effect of midodrine on chlorpromazine-induced orthostatic hypotension in rabbits: comparison with amezinium, etilefrine and droxidopa.

Orthostatic hypotension was produced in urethane-anesthetized rabbit by a combination of chlorpromazine (0.1 mg/kg, i.v.) and 45 degrees head-up tilt. The effect of midodrine (1 and 3 mg/kg, i.d.) was investigated in comparison with amezinium (10 and 30 mg/kg, i.d.), etilefrine (10 and 30 mg/kg, i.d.) and droxidopa (30 and 100 mg/kg, i.d.). The higher doses of each drug significantly mitigated the chlorpromazine-induced orthostatic hypotension, while none of the lower doses caused a significant effect. The effect of midodrine developed most rapidly; a significant effect was observed 25 min after administration. The order of onset time was midodrine < etilefrine < amezinium < droxidopa. The effect of droxidopa was significant only at 130 to 160 min after administration. The amplitude of effect was in the following order; midodrine = droxidopa > or = etilefrine > amezinium. Midodrine (3 mg/kg, i.d.) mitigated orthostatic hypotension induced by prazosin (0.1 mg/kg, i.v.), but not by pentolinium (0.6 mg/kg, i.v.). It is suggested that midodrine competes with chlorpromazine at alpha1-adrenoceptors and subsequently recovers reflex vasoconstriction. Midodrine may be useful to protect patients with impaired baroreflex activity from accidental orthostatic hypotension during treatment with neuroleptics.

Adrenergic alpha-Agonists↗
PubMed1989

Midodrine. A review of its pharmacological properties and therapeutic use in orthostatic hypotension and secondary hypotensive disorders.

Midodrine, a peripheral alpha-adrenergic agonist, finds use in the clinical management of patients with orthostatic hypotension or hypotension secondary to other clinical conditions or drug therapies. Midodrine is almost completely absorbed after oral administration and undergoes enzymatic hydrolysis to form its pharmacologically active metabolite, de-glymidodrine. In patients with refractory orthostatic hypotension oral midodrine increases standing blood pressure and improves symptoms of orthostatism, such as weakness, syncope, blurred vision and fatigue, without any associated cardiac stimulation. Comparative studies have shown midodrine to be clinically at least as effective as other sympathomimetic agents (norfenefrine, etilefrine, dimetofrine and ephedrine) and dihydroergotamine in this regard. Additionally, midodrine appears to cause less frequent and severe adverse effects associated with alpha-receptor agonism such as piloerection and urinary hesitancy. The most commonly experienced adverse effects--piloerector reactions, gastrointestinal disorders, and cardiovascular complaints--are generally mild and can be controlled by reducing the dosage of midodrine. Thus, midodrine is at least as useful as other currently available options in the management of orthostatic or secondary hypotension, and represents a stepping stone towards optimal therapy.

Animals↗
PubMed1996

Midodrine hydrochloride in patients on hemodialysis with chronic hypotension.

Chronic hypotension, volume nonresponsive, is not rare in hemodialysis patients and is usually refractory to various therapies. Midodrine hydrochloride is an alpha-mimetic drug acting directly on the peripheral alpha-receptor and increases blood pressure. We studied 10 uremic patients on hemodialysis with chronic hypotension to evaluate efficacy and safety of midodrine. Midodrine hydrochloride was administered at a dose of 2.5 mg twice on the dialytic day, 1.25 mg twice on the nondialytic day. Subjective symptoms and objective parameters were evaluated and compared before and after midodrine treatment. Midodrine significantly increased systolic pressure from 73.0 +/- 10.5 mm Hg to 90.5 +/- 12.3 mm Hg (p < 0.01); and diastolic blood pressure from 44.0 +/- 8.4 mm Hg to 55.4 +/- 7.9 mm Hg (p < 0.01) before dialysis. Orthostasis, dizziness, fatigue, blurred vision, dullness, headache, and depression improved an average of 62%. All patients tolerated midodrine treatment well. Only mild side effects were noted, including flush sensation, neck soreness, and headache. We conclude that midodrine may be another choice for uremic patients on hemodialysis with chronic hypotension which responds poorly to other conventional management.

Administration, Oral↗
PubMed2002

[Effects of midodrine on symptomatic hypotension during hemodialysis].

BACKGROUND: Hypotension occurs in 20% of hemodialysis procedures. AIM: To study the effects of midodrine on hypotension during hemodialysis. PATIENTS AND METHODS: Ten patients on chronic hemodialysis and with a history of hypotension during the procedure, were studied. They received midodrine 10 mg per os or placebo during 5 dialytic procedures each, in a double blind cross over design. RESULTS: Blood pressure levels prior to dialysis were similar during the midodrine or placebo administration periods. During dialysis, systolic blood pressure fell 19.3 +/- 28 mmHg with midodrine and 23.4 +/- 28 mmHg with placebo. Diastolic blood pressure fell 7.3 +/- 11.5 mmHg with midodrine and 11.1 +/- 12 mmHg with placebo. The reduction in median arterial pressure was also less pronounced with midodrine. CONCLUSIONS: Midodrine lessens the fall in arterial pressure during hemodialysis, in patients with symptomatic hypotension.

Adrenergic alpha-Agonists↗
PubMed1986

Effects of midodrine on experimentally-induced postural hypotension in dogs.

Effects of alpha-(2,5-dimethoxyphenyl)-beta-glycinamide-ethanol hydrochloride (midodrine, ST-1085) on experimental postural hypotension was examined in hexamethonium (20 mg/kg s.c.)-treated anesthetized dogs. The dogs were tilted 30 degrees to a head-up position. A 30 degree-tilt caused a significant decrease in blood pressure. Midodrine, 0.3 mg/kg, attenuated the decrease in blood pressure induced by the tilt significantly at 10 and 30 min after administration of the drug. The heart rate increased following the tilt, but the degree of the increase was rather small. Cerebral tissue blood flow significantly decreased by the tilt. Midodrine, 0.3 mg/kg, significantly attenuated the decrease in cerebral tissue blood flow induced by the tilt at 10 and 30 min. Vertebral arterial blood flow significantly decreased by the tilt. Midodrine reduced the decrease in vertebral arterial blood flow induced by the tilt significantly at 10 and 30 min. Cardiac output also decreased significantly by the tilt. Midodrine attenuated the decrease in cardiac output significantly at 10 min. Femoral arterial blood flow decreased significantly by the tilt. Midodrine tended to reduce the decrease in femoral arterial blood flow induced by the tilt at 30 min. Therefore, midodrine via vasoconstriction seems to be useful for the decrease in blood flows due to the postural hypotension.

Adrenergic alpha-Agonists↗
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↗
PubMed1996

Midodrine treatment for patients with hemodialysis hypotension.

Hypotension is the principal complication of chronic hemodialysis. Autonomic insufficiency is thought to be a primary contributing cause of hemodialysis hypotension. We treated patients who experience hemodialysis hypotension with midodrine, a selective alpha-1 adrenergic pressor agent in an initial effort to assess potential efficacy. Twenty-one patients who experienced severe hypotension during hemodialysis participated in this study. To qualify, patients had to exhibit a fall of > or = 30 mmHg in systolic blood pressure with associated clinical symptoms during hemodialysis. The lowest intra- and post-dialysis blood pressures were monitored for five consecutive hemodialysis treatment periods before receiving midodrine, as a baseline. After the patients were titrated to a maintenance midodrine dose, the lowest intra- and post-dialysis blood pressure data were again collected for five consecutive dialysis treatments. Hemodialysis blood pressures on midodrine treatment were compared to baseline to evaluate the effect of midodrine. Midodrine given at a mean treatment dose of 8 mg (range 2.5-25) significantly increased the mean (+ or - SE) minimal systolic pressure from 93.1 "+ or - " 3.8 to 107.1 + or - 3.2 mmHg (p <0.01) and elevated the mean diastolic pressure from 52.3 + or - 2.9 to 57.9 + or - 2.3 mmHg during hemodialysis. Also, the post-dialysis blood pressures (systolic/diastolic) were significantly increased from 115.6 + or - 3.1/62.3 + or - 2.1 to 129.9 + or - 3.9/68.1 + or - 1.7 mmHg (p <0.01 and 0.05, respectively). No apparent clinical or laboratory abnormalities were observed. Oral midodrine appears to be a safe and effective therapy for the treatment of hemodialysis hypotension.

Adrenergic alpha-Agonists↗
PubMed2002

Midodrine in neurally mediated syncope: a double-blind, randomized, crossover study.

Neurally mediated syncope is the most frequent cause of syncope in patients without structural heart disease. Its most common trigger is a reduction in venous return to the heart due to excessive venous pooling in the legs. We conducted a double-blind, randomized, crossover trial to investigate the efficacy of midodrine, a selective alpha-1 adrenergic agonist that decreases venous capacitance, in preventing neurally mediated syncope triggered by passive head-up tilt. Twelve patients with history of recurrent neurally mediated syncope, which was reproduced during head-up tilt, were randomized to receive a nonpressor dose of midodrine (5mg) or placebo on day 1 and the opposite on day 3. One hour after drug or placebo administration, patients underwent 60-degree head-up tilt lasting 40 minutes (unless hypotension or bradycardia developed first). In the supine position, midodrine produced no significant change in blood pressure or heart rate. The responses to head-up tilt were significantly different on the midodrine and the placebo day: on the placebo day, 67% (8/12) of the subjects suffered neurally mediated syncope, whereas only 17% (2/12) of the subjects developed neurally mediated syncope on the midodrine day (p < 0.02). These results indicate that midodrine significantly improves orthostatic tolerance during head-up tilt in patients with recurrent neurally mediated syncope.

Adult↗
PubMed2000

Preliminary experience with midodrine in kidney/pancreas transplant patients with orthostatic hypotension.

In an effort to ameliorate the problem of orthostatic hypotension in pancreas transplant patients, current medical management consists of maximizing the patient's hydration, altering antihypertensives, increasing sodium intake, initiation of fludrocortisone, compression stockings, and behavioral modifications. Despite these medical interventions, a subset of patients remains symptomatic. Midodrine (ProAmatine), an alpha-adrenergic agonist, was approved for the treatment of symptomatic orthostatic hypotension in the US. This preliminary report attempts to assess the safety and efficacy of midodrine use in kidney/pancreas (KP) or pancreas alone (PA) transplant recipients. A retrospective review was performed of 7 KP and 1 PA recipient experiencing symptomatic postural hypotension after maximizing other medical treatments. Blood pressure, serum creatinine (SrCr), and objective responses to postural hypotension were assessed at routine intervals. Pre-midodrine monitoring revealed a mean orthostatic change in systolic blood pressure from sitting to standing of 43 mmHg (range 20-100 mmHg). Patients received a mean starting midodrine dose of 18 mg/d, which was titrated to a maximum dose of 30 mg/d. Systolic blood pressure monitoring revealed a mean orthostatic change of 27 mmHg (range 0-81 mmHg) after initiation of treatment with midodrine and a mean follow-up of 3.2 months. All study patients reported improvement in symptoms of orthostatic hypotension. SrCr was not affected based upon comparison of pre-treatment and current SrCr values of 1.4 and 1.3 mg/dL, respectively. The most common side effect experienced was supine hypertension. These preliminary results suggest that midodrine is safe and effective in transplant recipients; however, the dosage should be titrated to symptomatic relief or a maximum dose of 30 mg. Careful monitoring for supine hypertension is necessary.

Adrenergic alpha-Agonists↗
PubMed2003

Midodrine improves chronic hypotension in hemodialysis patients.

BACKGROUND: The effects of midodrine on chronic hypotension in hemodialysis (HD) patients have not been well investigated. METHODS: We evaluated midodrine's effect on autonomic function and hemodynamics in 12 HD patients who had chronic systolic blood pressure less than 100 mm Hg. Midodrine (5.0 mg) twice a day was given for 4 weeks. Another 12 age- and sex-matched HD patients with normotension were selected as a control group. Autonomic function tests included the heart-rate responses to the Valsalva maneuver and 30:15 ratio as well as supine and standing blood pressure (BP) and sustained hand-grip test. Hemodynamic changes included 24-hour blood pressure, cardiac output, total peripheral resistance (TPR), and plasma renin and aldosterone concentrations. RESULTS: Compared with the control subjects, HD patients with chronic hypotension had more severe autonomic dysfunction and significantly lower TPR. After 4 weeks of midodrine therapy, sympathetic function (orthostatic and hand-grip tests) improved in conjunction with significant increases in mean arterial pressure (MAP) (79.5 +/- 4.9 to 85.0 +/- 5.1 mm Hg, P < 0.05) and TPR (768 +/- 37 versus 1097 +/- 72 dyne/sec/cm-5, P < 0.01) despite no significant change in Valsalva ratio, 30:15 ratio, and cardiac output. MAP changes were positively correlated with TPR changes (r = 0.82, P < 0.001). Supine plasma renin activity was significantly increased. In addition, MAP during HD was also significantly increased during midodrine therapy. CONCLUSIONS: Midodrine improves chronic hypotension in HD patients by modulating autonomic function and its direct effects on peripheral vessels.

Adrenergic alpha-Agonists↗
PubMed1997

Efficacy of midodrine hydrochloride in neurocardiogenic syncope refractory to standard therapy.

INTRODUCTION: Some patients with neurocardiogenic syncope continue to have recurrent syncope or presyncope despite the use of currently available drug therapy. The purpose of this study was to determine whether midodrine hydrochloride, a selective adrenergic agonist, could be effective in patients resistant to, or intolerant of, currently used medications in the treatment of neurocardiogenic syncope. METHODS AND RESULTS: Eleven patients with a history of recurrent syncope or presyncope in whom hypotension with syncope or presyncope could be provoked during head-up tilt testing were included. There were 4 men and 7 women with a mean age (+/-SD) age of 34 +/- 13 years. In all patients, standard therapy with beta-adrenergic receptor blocking agents, ephedrine, theophylline, disopyramide, fludrocortisone, and sertraline hydrochloride, was either ineffective, poorly tolerated, or contraindicated. Midodrine was initially administered orally at a dose of 2.5 mg three times daily. After adjustment of dosage over 2 to 4 weeks, patients were followed-up clinically. Midodrine was discontinued in one patient because of side effects. Frequency of syncope or presyncope during the 3 months prior to starting treatment was compared during a mean follow-up of 17 +/- 4 weeks after starting treatment with midodrine. There was significant (P < 0.01) reduction in syncopal and presyncopal episodes on midodrine. Five patients had complete resolution of symptoms, while four patients had significant improvement. Symptoms did not improve in one patient. CONCLUSIONS: Midodrine hydrochloride can be effective in preventing recurrent symptoms in selected patients with neurocardiogenic syncope unresponsive to, or intolerant of, standard drug therapy.

Administration, Oral↗
PubMed2005

The effects of chronic treatment with octreotide versus octreotide plus midodrine on systemic hemodynamics and renal hemodynamics and function in nonazotemic cirrhotic patients with ascites.

OBJECTIVES: The adrenergic agonist midodrine improved circulatory and renal dysfunction when acutely administered in nonazotemic cirrhotic patients with ascites while its combination with octreotide has recently been proposed as an effective treatment of type 1 hepatorenal syndrome (HRS). However, the effects of octreotide on systemic hemodynamics and renal function in cirrhotic patients are controversial. This study evaluated the effects of chronic treatment with octreotide versus octreotide plus midodrine on systemic hemodynamics and renal hemodynamics, and function in nonazotemic cirrhotic patients with ascites. METHODS: Twenty-five patients were studied at baseline and 11 days after administration of subcutaneous octreotide 300 mug, b.i.d. alone (n = 12) or together with oral midodrine 7.5 mg, t.i.d. (n = 13). RESULTS: Octreotide did not improve systemic hemodynamics whereas the addition of midodrine significantly decreased cardiac index (CI) and heart rate (HR), and increased mean arterial pressure (MAP) and systemic vascular resistance (SVR). Octreotide caused a decrease in renal vascular resistance (RVR) and increased renal blood flow (RBF) but significantly reduced glomerular filtration rate. The association of midodrine to octreotide did not modify renal hemodynamics and function as compared to baseline while it caused an almost significant minor increase in RVR and a significant minor decrease in RBF as compared to octreotide alone. Consequently, a significant minor increase in glomerular filtration rate was demonstrated. The plasma values of active renin, aldosterone, and glucagon were significantly reduced in either group. CONCLUSIONS: Octreotide does not improve systemic hemodynamics in nonazotemic cirrhotic patients with ascites while it impairs renal function. On the other hand, the addition of midodrine can ameliorate the hyperdynamic circulation without inducing renal dysfunction in these patients.

Administration, Oral↗
PubMed1997

Midodrine for the treatment of intradialytic hypotension.

Recurrent intradialytic hypotension is probably the most severely disabling feature in dialysis patients and the etiology is multifactorial. We assessed the efficacy and safety of midodrine, a selective alpha1-adrenergic pressor agent in 12 patients with recurrent intradialytic hypotension. Symptomatic intradialytic hypotension was defined as hypotensive symptoms occurring with a systolic blood pressure < 100 mm Hg or with 25% decrease in systolic blood pressure in those patients with a basal systolic blood pressure of 100 mm Hg. The patients who suffered from symptomatic intradialytic hypotension and failed to improve after cautious body weight adjustment were included into the study. The lowest intradialytic and postdialysis blood pressures were monitored for 18 consecutive dialysis sessions before and after midodrine treatment. Clinical signs and symptoms were also recorded during both periods. With midodrine, the mean (+/- SE) lowest systolic and diastolic blood pressure increased significantly from 68.7 +/- 3.1 and 42.8 +/- 2.0 mm Hg to 84.7 +/- 3.9 and 52.7 +/- 2.7 mm Hg respectively during the study (p < 0.01). Midodrine treatment also significantly increased postdialysis systolic and diastolic blood pressures from baseline values of 90.8 +/- 3.8 and 58.3 +/- 3.0 mm Hg to 113.3 +/- 7.1 and 70.6 +/- 3.1 mm Hg (p < 0.01 and p < 0.01 respectively). In addition, oral administration of midodrine also significantly decreased the total volume of intravenous fluid administered during symptomatic hypotension. The clinical signs and symptoms during dialysis were improved in all patients. There were no differences in hemoglobin, serum albumin, urea, creatinine, fasting blood sugar or volume removed per dialysis between both periods of the study. In conclusion, our study has demonstrated that midodrine is a safe and effective treatment for the prevention of recurrent intradialytic hypotension if routinely premedicated before each dialysis session.

Administration, Oral↗
PubMed1984

Controlled clinical investigation of dimetophrine versus midodrine in the management of moderately decreased arterial blood pressure.

An open, controlled study was carried out in 30 in-patients with low arterial pressure syndrome to compare the effectiveness and tolerance of dimetophrine and midodrine in restoring blood pressure to normal levels and relieving symptoms. Patients were allocated at random to receive treatment for 15 days with either 100 mg dimetophrine tablets or 2.5 mg midodrine tablets and dosage was adjusted according to each patient's condition. Blood pressure and heart rate were monitored daily, symptoms were assessed every 8 days, and laboratory tests carried out before and after treatment. The results showed that both drugs significantly increased systolic and diastolic pressure to normal levels during the trial period and no patient failed to respond. Dimetophrine showed a significantly faster onset of action in increasing systolic pressure and levels reached a plateau significantly earlier than with midodrine. No significant differences were observed between the effects of the two drugs on diastolic pressure, although there was a smoother and more progressive increase in dimetophrine-treated patients. Neither drug significantly modified the heart rate. Both drugs were effective in relieving symptoms but, although there was no significant difference between treatments, patients on dimetophrine experienced somewhat faster and greater relief than those receiving midodrine. At the end of the treatment period, only 11% of dimetophrine-treated patients still complained of mild symptoms compared with 33% of those on midodrine. The mean daily dosage was 3.7 tablets of dimetophrine and 4.9 tablets of midodrine. Both drugs were well tolerated; no side-effects were reported and there were no abnormalities in the laboratory tests.

Adult↗
PubMed1998

Midodrine. A review of its therapeutic use in the management of orthostatic hypotension.

Midodrine is a prodrug which undergoes enzymatic hydrolysis to the selective alpha 1-adrenoceptor agonist desglymidodrine after oral administration. Oral midodrine significantly increases 1-minute standing systolic blood pressure compared with placebo. The drug also improves standing time and energy level and clinical symptoms of orthostatic hypotension including dizziness, light-headedness and syncope. Comparative studies have shown midodrine to have similar efficacy to dihydroergotamine mesylate, norfenefrine, fludrocortisone and etilefrine, and to be more effective than dimetofrine and ephedrine in patients with orthostatic hypotension. Midodrine is well tolerated, with the most commonly reported adverse events being piloerection, pruritus, paraesthesias, urinary retention and chills. The risk of supine hypertension, which is associated with midodrine therapy in up to 25% of patients, can be reduced by taking the final daily dose at least 4 hours before bedtime. Thus, oral midodrine is an effective therapeutic option for the management of various forms of orthostatic hypotension. This well-tolerated agent is likely to be useful in conjunction with standard nonpharmacological care.

Adrenergic alpha-Agonists↗
PubMed2006

Hemodynamic effects of midodrine after spaceflight in astronauts without orthostatic hypotension.

INTRODUCTION: Orthostatic hypotension and presyncope are common and potentially serious risks for astronauts returning from space. Susceptible subjects fail to generate an adequate adrenergic response to upright posture. The alpha-1 adrenergic agonist, midodrine, may be an effective countermeasure. We tested the hypothesis that midodrine would have no negative hemodynamic effect on healthy astronauts returning from space. METHODS: Five male astronauts participated in preflight and post-flight tilt testing on a control flight as well as on the test flights, where midodrine (10 mg, orally) was administered after landing approximately 1 h before testing. RESULTS: None of these astronauts exhibited orthostatic hypotension or presyncope before or after either flight. Midodrine did not cause any untoward reactions in these subjects before or after flight; in fact, a modest beneficial effect was seen on postflight tachycardia (p = 0.036). DISCUSSION: These data show that midodrine protected against post-spaceflight increases in heart rate without having any adverse hemodynamic effects on non-presyncopal, male astronauts. Among these subjects, midodrine was a safe cardiovascular countermeasure.

Adrenergic alpha-Agonists↗