Generic Imdur is an effective medication which helps in the treatment of angina attacks. Generic Imdur acts as nitrates.
Other names for this medication:
Also known as: Isosorbide Mononitrate.
Generic Imdur is a perfect remedy, which helps to treat angina attacks.
Generic Imdur acts as nitrates.
Imdur is also known as Isosorbide Mononitrate.
Generic name of Generic Imdur is Isosorbide Mononitrate.
Brand names of Generic Imdur are Imdur, ISMO, Monoket.
Take Generic Imdur tablets orally with or without food.
Do not crush or chew it.
Take Generic Imdur at the same time with water.
If you want to achieve most effective results do not stop taking Generic Imdur suddenly.
If you overdose Generic Imdur and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Imdur are difficult or slow breathing, muscle cramps, nausea, vomiting, diarrhea, high temperature, fainting, abnormal heartbeat, changes in vision, flushing, convulsions, severe throbbing migraine, lightheadedness.
Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.
The most common side effects associated with Imdur are:
Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.
Do not take Generic Imdur if you are allergic to Generic Imdur components.
Do not take Generic Imdur if you're pregnant or you plan to have a baby.
Do not use potassium supplements or salt substitutes.
Be careful using Generic Imdur if you take dihydroergotamine (D.H.E. 45); or any other heart medicines, especially those used to treat high blood pressure or irregular heartbeats.
Be careful using Generic Imdur if you suffer from or have a history of congestive heart failure, have low blood pressure; a stroke, a transient ischemic attack (TIA, or mini-stroke), have anemia; have an allergy to nitrates; have closed-angle glaucoma; migraines, kidney disease; liver disease, heart attack, a serious head injury.
If you want to achieve most effective results without any side effects it is better to avoid alcohol.
Be very careful when you are driving machine.
Do not stop taking Generic Imdur suddenly.
In this double-blind, randomized, placebo-controlled cross-over study, the authors investigated the initial time course of effects of isosorbide-5-mononitrate (IS-5-MN) on hemodynamic parameters in 15 healthy male volunteers after administering a single oral dose of either an immediate-release formulation (IS-5-MN 20 mg) or of a sustained-release formulation (IS-5-MN 50 mg). The latter formulation released 15 mg IS-5-MN immediately, while 35 mg of the dose was sustained release. The onset of effect on the a/b-ratio of the finger pulse curve (20 minutes after administration) and on heart rate following orthostatic challenge (30 minutes) was not different following ingestion of either the immediate-release or the sustained-release formulation. Only the systolic blood pressure following orthostatic challenge was affected earlier after ingestion of the immediate-release form of IS-5-MN (10 vs. 30 minutes). There was no statistically significant difference in the maximum effect on the measured hemodynamic parameters between the two formulations. There was no significant difference with respect to the effect per dose between both of the active treatments (i.e., IS-5-MN 20 mg immediate release and IS-5-MN 50 mg sustained release) within 6 hours after administration. The hemodynamic findings were consistent with the observed rates of the increase of plasma concentrations of IS-5-MN following both formulations. Thus, the administration of the sustained-release formulation of IS-5-MN 50 mg caused similar maximum effects when compared with an immediate-release formulation (20 mg). While the onset of effect of IS-5-MN on the a/b-ratio of the finger pulse curve and on heart rate following orthostasis was similar after administration of either the immediate- or the sustained-release formulation, the onset of effect of the sustained-release formulation on systolic blood pressure orthostasis was determined slightly later. However, the latter difference seems to be of minor clinical relevance.
ISMN preparations can be recommended as monotherapy in patients of FC II-III angina or in combination with beta adrenoblockers for treatment of patients with angina FC III-IV.
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The haemodynamic effects of 10 mg of isosorbide-5-mononitrate (IS-5-MN) and 10 mg of isosorbide dinitrate (ISDN), administered in intravenous injection, were compared in 16 patients with acute myocardial infarction. The study, using the balloon thermodilution catheter, took 4 hours to complete. Both drugs produced a decrease in pulmonary and peripheral arterial pressure, cardiac index, stroke and stroke work indexes; the effect was present immediately after administration to reach a maximum 3-15 minutes later, after which the values gradually returned to baseline levels. While IS-5-MN resulted in an increase in peripheral arterial resistance, heart rate rose briefly following the administration of ISDN. After IS-5-MN, pulmonary diastolic pressure decreased by 15% and peripheral arterial pressure by 5%, and stroke work index by 12%; the magnitude of decrease was double following the administration of ISDN (30%, 15% and 23%, respectively). The decrease in cardiac and stroke indexes was likewise less pronounced after IS-5-MN than after ISDN, the difference, however, was not statistically significant. Duration of the haemodynamic effect of both drugs was about the same--approximately 3 hours.
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To determine whether patients receiving isosorbide 5-mononitrate (ISMN) use the drug in a pharmacologically appropriate manner and whether they had been instructed in the prophylactic use of sublingual nitrates prior to effort.
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Nitrate therapy improves hemodynamics in patients with heart failure, but the chronic effects of oral nitrates on exercise performance and clinical status have not been well studied.
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Patients who have bleeding from esophageal varices are at high risk for rebleeding and death. We compared the efficacy and safety of endoscopic sclerotherapy with the efficacy and safety of nadolol plus isosorbide mononitrate for the prevention of variceal rebleeding.
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In the management of the patient with chronic cardiac failure, the combination of an arteriolar vasodilator and venodilator should be beneficial. 8 patients with NYHA grade III-IV chronic cardiac failure were studied following placebo, after 4 weeks' therapy with the arteriolar vasodilator felodipine, and with the combination of felodipine and oral isosorbide 5-mononitrate. Haemodynamic measurements were made at rest and during dynamic exercise at an individual, fixed, near maximal workload. Ejection fraction (EF) was obtained by gated radionuclide ventriculography. At rest, heart rate was unchanged 73 +/- 6 at control, 72 +/- 4 with felodipine and 74 +/- 4 beats/min with the addition of isosorbide 5-mononitrate. Mean arterial pressure fell from 98 +/- 5 to 84 +/- 4 (p less than 0.02) and 84 +/- 3 mm Hg (p less than 0.02) with nitrate. Cardiac index increased from 2.2 +/- 0.1 to 2.5 +/- 0.2 litres/min/m2 with felodipine and further to 2.6 +/- 0.2 litres/min/m2 (p less than 0.02) with nitrate. Exercise tachycardia and mean arterial pressure were not significantly affected by therapy. Cardiac index increased on exercise from 4.4 +/- 0.3 to 4.8 +/- 0.3 litres/min/m2 with felodipine and 4.9 +/- 0.3 litres/min/m2 (p less than 0.05) with the addition of nitrate. Stroke volume index increased from 35.4 +/- 4 to 40.8 +/- 4 beats/min/m2 and further to 41.0 +/- 4 beats/min/m2 (p less than 0.05) and EF from 14 +/- 3 to 18 +/- 3% with nitrate. In conclusion, in patients with chronic cardiac failure, treatment with a calcium channel blocker produced sustained haemodynamic improvement, particularly on exercise, and combination with nitrate produced further benefit.
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Both monotherapy with amlodipine and diltiazem (Adizem XL) were effective on symptoms and ambulatory and exercise ischemia. Combination therapy reduced ischemia further, with amlodipine/atenolol superior to diltiazem (Adizem XL)/isosorbide 5-mononitrate. Amlodipine/atenolol was significantly superior during the drug-free interval with maintenance of ischemia reduction.
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The major aim of this study was to prepare isosorbide-5-mononitrate (5-ISMN) sustained-release pellets and evaluate their stability. The pellets were prepared by extrusion/spheronization, and then the core pellets were coated with ethylcellulose (EC 10cp) and Eudragit(®)NE30D. Here, EC was used as the subcoating agent while Eudragit(®)NE30D acted as the outer-coating agent. 5-ISMN sustained-release pellets as a novel drug delivery system contained the immediate-release portion in the outer-coating layer. Unexpectedly, 5-ISMN was found to migrate from the interior of the pellets to the surface forming needle crystals and exhibited the phenomenon of sublimation, which resulted in a tremendous increase in the release rate. Our research showed that the migration and sublimation of the active ingredient was related to the temperature and humidity. Polyvinylpyrrolidone (PVP K30) can affect the precipitation of 5-ISMN by forming a charge transfer complex between the drug and PVP, while hydroxypropyl methyl cellulose (HPMC E5) had no effect, and confirmed the correctness of this view through photographs and IR spectra. In the investigation of the stability, the results showed that there was no sublimation and migration while the pellets stored at 25°C/60%RH (ambient conditions) and 40°C/75% RH (stress conditions) during a 6-month period.
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Coadministration of sildenafil with ISMN or GTN produced significantly greater reductions in BP than ISMN or GTN alone. Based on these data, sildenafil should not be administered to patients taking nitrates.
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Dogs were subjected to various durations of ventricular tachypacing (VTP, 220 to 240 bpm) in the presence or absence of oral enalapril 2 mg. kg(-1). d(-1). VTP for 5 weeks induced CHF, local atrial conduction slowing, and interstitial fibrosis and prolonged atrial burst pacing-induced AF. Atrial angiotensin II concentrations and MAPK expression were increased by tachypacing, with substantial changes in phosphorylated forms of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38-kinase. Enalapril significantly reduced tachypacing-induced changes in atrial angiotensin II concentrations and ERK expression. Enalapril also attenuated the effects of CHF on atrial conduction (conduction heterogeneity index reduced from 3.1+/-0.4 to 1.9+/-0.2 ms/mm, P<0.05), atrial fibrosis (from 11.9+/-1.1% to 7.5+/-0.4%, P<0.01), and mean AF duration (from 651+/-164 to 218+/-75 seconds, P<0.05). Vasodilator therapy of a separate group of VTP dogs with hydralazine and isosorbide mononitrate did not alter CHF-induced fibrosis or AF promotion.
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The optimal medical therapy for ischemia suppression and the impact of irregular dosing using agents with different pharmacologic properties has not been established in patients with coronary disease.
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In this report, we investigated the combined effect of drug liposomalization and addition of glycerol on the transdermal delivery of isosorbide 5-nitrate (ISN) in rat abdominal skin in vitro. Occlusive application of both liposomal and aqueous ISN solution, with and without addition of 5% glycerol, showed that drug liposomalization and addition of glycerol has far-reaching implications for ISN permeation and accumulation in 4 and 8 weeks old rat abdominal skin. Using 8 weeks old rat abdominal skin, the optimal concentration of glycerol to be added to liposomal ISN was found to be 5%. The ISN mean values permeated through and accumulated in stripped 8 weeks old rat abdominal skin from those formulations described above were not significant different, which might indicate the combined effect of glycerol and liposomal ISN resides solely in the stratum corneum (SC). Based on previous reports, the enhancement effect of glycerol might be due to an increase in the SC hydration, and perhaps due to subtle changes in the lipid organization caused by penetration of liposomal lipids within the SC intercellular spaces. These data might provide evidence that glycerol action on SC is useful to facilitate skin permeation and accumulation of drugs formulated in liposome.
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Four treatment groups were comparable regarding baseline characteristics. Esophageal variceal rebleeding occurred in 22% patients in band ligation plus drugs group, 26% patients in drug combination group, 31% patients in banding group and 38% patients in propranolol group (p=0.41). Difference in mortality rates was also not significant.
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To estimate whether vaginal isosorbide mononitrate, added to oral misoprostol for cervical ripening and labor induction, shortens time to vaginal delivery.
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A single and 5-d-repeated oral doses of 5-IM 50 mg were performed on 2 groups of 20 Chinese healthy subjects (10 subjects for each group) in a randomized crossover protocol. The 5-IM in plasma were measured by gas chromatography with electron-captured detector method. Data were analyzed automatically by using a CAPP program on a PC computer.
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Long-term exposure to organic nitrates influences different sections of the vascular bed heterogeneously. Continuous dosage of nitrates leads to the development of tolerance both to the vascular effects and to the unwanted adverse effect, headache. Human data on the development of tolerance in different cranial arteries over more than 24 h are lacking. We compared the vascular changes of the middle cerebral, superficial temporal and radial arteries during oral administration of isosorbide-5-mononitrate (5-ISMN) 30 mg three times daily for 7 days in 11 healthy subjects in a double-blind, randomised, placebo controlled cross-over design. Blood velocity in the middle cerebral artery was measured with transcranial Doppler and the diameters of the temporal and radial arteries were measured with high frequency ultrasound. Headache recordings were compared to the observed vascular changes over time. Tolerance was complete within 24 h in the middle cerebral artery whilst in the superficial temporal and the radial arteries, tolerance was only partial and developed much more slowly, i.e. after 7 days correlating with the disappearance of NO-induced headache. The present study thus demonstrated the important differences in the time profiles of appearance of nitrate tolerance in arteries of different vascular beds in man. If vasodilatation is the cause of NO-induced headache the results point to extracerebral arteries as the locus of nociception. Due to a variety of other possible pain-inducing effects of nitric oxide our results do not exclude cerebral arteries.
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We document for the first time that IS-5-MN impairs endothelial function in humans in vivo. Suggesting a role of oxygen free radicals, nitrate-induced abnormalities in endothelium-dependent vasomotor responses were reversed by the antioxidant vitamin C.
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Nicorandil is beneficial as treatment for AP.
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Isosorbide dinitrate 10 mg, isosorbide 5-mononitrate 5 mg and isosorbide 2-mononitrate 5 mg were administered orally to subjects with and without renal failure, and the plasma concentrations of isosorbide dinitrate and of both the mononitrates were measured. There was no striking difference in plasma concentration as a function of time between subjects with and without renal failure, except for a somewhat higher isosorbide 5-mononitrate concentration after administration of this metabolite to uraemic patients.
The administration of ISMO causes a decrease in ERPF in cirrhotic patients and its use in patients with renal impairment should be considered cautiously.
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