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.
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This study investigates the mechanisms of platelet inhibition by the nitrate esters isosorbide dinitrate, isoidide dinitrate, isomannide dinitrate, isosorbide 2-mononitrate and isosorbide 5-mononitrate as compared to the spontaneous nitric oxide (NO)-donor linsidomine, the active metabolite of molsidomine. Nitrates and linsidomine dose-dependently inhibited aggregation, ATP secretion and thromboxane formation of washed human platelets at a rank order of potency, identical with that for stimulation of cyclic GMP in cultured rat lung fibroblasts. While linsidomine (0.1 mM) caused a 3-fold platelet cGMP elevation, there was a weak (< or = 30%) but significant cGMP stimulation by organic nitroesters, which was tightly correlated with inhibition of platelet aggregation (r = 0.926, P = 0.008). Zaprinast (2 microM) potentiated, while methylene blue (1 microM) and oxyhemoglobin (10 microM) reversed the antiaggregatory effects. Linsidomine (0.5 microM-0.1 mM) dose-dependently released NO in a cell-free system. No spontaneous NO release was detected with organic nitroesters (0.1 mM). These data suggest that, to some extent, bioactivation of organic nitroesters occurs in platelets, resulting in platelet inhibition via the NO/cGMP system.
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Cepharanthin (CEP) is a biscoclaurine alkaloid extracted from Stephania cepharantha Hayata. CEP is reported to inhibit drug resistance by inhibiting P-glycoprotein, a drug efflux pump, and recently to induce apoptosis. In the present study, we examined the effects of CEP as an inhibitor of adriamycin (ADR) resistance on ADR-induced apoptosis and necrosis. First, we established p53-deficient ADR-resistant osteosarcoma cell lines, SaOS2-AR and SaOS2 F-AR. Resistant cells showed a higher level of intracellular glutathione peroxidase activity than parent cells. P-glycoprotein was overexpressed in resistant cells. The intracellular ADR level of resistant cells was lower than that of parent cells. One micro g/ml CEP eliminated the degradation of intracellular ADR of resistant cells; that is, to a level equivalent to that of the parent cells. CEP of 0.5 micro g/ml, which was not cytotoxic when used alone, significantly increased the ADR sensitivity of resistant cells, to a level similar to the parent cell level. Isosorbide 5-mononitrate, a potential nitric oxide-generation agent, combined with CEP further increased the ADR sensitivity of resistant cells, indicating a synergistic effect of CEP and isosorbide 5-mononitrate on ADR cytotoxicity. Time-lapse microscopic observation revealed that ADR dominantly induced apoptosis much more than necrosis for both parent and resistant cells, and that the use of 0.5 micro g/ml CEP with ADR synergistically accelerated apoptosis in resistant cells. Finally, we clarified the property by which CEP synergistically accelerates ADR-induced apoptosis. This property might be a new mechanism that explains how CEP overcomes ADR resistance.
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Rats dosed orally with isosorbide dinitrate (1 mg kg-1) were exposed to smoke from standard and nicotine-reduced cigarettes for 8 min using a smoking machine. Plasma concentrations of isosorbide dinitrate and 5-isosorbide mononitrate, one of its major metabolites were approximately equal in the exposed groups, but were lower than in the non-smoking control group. The 2-isosorbide mononitrate concentration was also lower in the group exposed to smoke from standard cigarettes. Since the pharmacokinetics were influenced by smoke from both types of cigarette smoke, the effect may be attributed in large part to non-nicotine components of the smoke.
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To compare the efficacy of a nitric oxide donor (isosorbide mononitrate) and a prostaglandin E1 analogue (misoprostol) for cervical priming before suction termination of pregnancy.
We performed a multicenter, randomized, double-blind, phase III, placebo-controlled trial in 154 patients aged over 65 years with refractory isolated systolic hypertension. Patients were randomized to placebo or 40 mg/day of extended-release isosorbide mononitrate added to standard therapy and titrated to 60 mg/day at week 6 if blood pressure exceeded 140/90 mmHg.The primary objective was to assess the effect on clinical pulse pressure of extended-release isosorbide mononitrate added to standard therapy in patients aged over 65 years with refractory isolated systolic hypertension after 3 months of treatment.The secondary objectives were as follows: to quantify the effect of adding the study drug on central blood pressure and vascular compliance using the augmentation index and pulse wave velocity; to evaluate the safety profile by recording adverse effects (frequency, type, severity) and the percentage of patients who had to withdraw from the trial because of adverse events; to quantify the percentage of patients who reach a clinical systolic blood pressure <140 mmHg or <130 mmHg measured by ambulatory blood pressure monitoring; and to quantify the change in pulse pressure measured by ambulatory blood pressure monitoring.
Both medical therapy and endoscopic variceal ligation (EVL) have proven to be comparable in the prevention of variceal rebleeding. However, the long-term results are still lacking. Our previous study enrolled 121 patients with history of esophageal variceal bleeding and randomized to receive EVL (EVL group, 60 patients) or drug therapy, nadolol plus isosorbide-5-mononitrate (N+I) (N+I group, 61 patients) to prevent variceal rebleeding. The EVL group received ligation regularly until variceal obliteration. The N+I group received N+I during the study period. Patients were followed for up to 8 years. After a median follow-up of 82 months, recurrent upper gastrointestinal bleeding developed in 28 patients (47%) in the EVL group and 49 patients (80%) in the N+I group (P = 0.001). Recurrent bleeding from esophageal varices occurred in 18 patients (30%) in the EVL group and 39 patients (64%) in the N+I group. The actuarial probability of rebleeding from esophageal varices was lower in the EVL group (P = 0.001). A total of 42 patients of the EVL group and 30 patients of the N+I group died (P = 0.013). The multivariate Cox analysis indicated that age, serum albumin, presence of encephalopathy, and treatment were the factors predictive of mortality.
Databases, references and meeting abstracts were searched to retrieve randomized trials comparing combined therapy with EVL and β-blockers ± ISMN vs either treatment alone, to prevent variceal rebleeding in cirrhosis. Random-effects model was used for meta-analysis.
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to compare effects of isosorbide dinitrate, isosorbide-5-mononitrate and nicorandil on frequency of angina attacks and vasoregulating endothelial function in patients with ischemic heart disease (IHD). MATERIAL AND METHODS. In 117 patients with stable II-III functional class angina we analyzed frequency of angina attacks, exercise tolerance, data of 24-hour Holter ECG monitoring and brachial artery Doppler study. RESULTS. Patients with IHD had impaired endothelium-dependent vasodilation in the form of reduced endothelial response to increase of "shear stress" during test with reactive hyperemia. Long-term therapy with isosorbide dinitrate, isosorbide-5-mononitrate, and nicorandil was associated with normalization of endothelium-dependent vasodilation of the brachial artery. This effect was more pronounced during therapy with nicorandil.
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This study was performed to compare the pharmacokinetic properties and relative bioavailability of two isosorbide-5-mononitrate (5-ISMN) sustained-release drugs in healthy Korean subjects under fasting and fed conditions.
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Cirrhosis can be the end stage of any chronic liver disease. At the time of diagnosis of cirrhosis varices are present in about 60% of decompensated and 30% of compensated patients. The risk factors for the first episode of variceal bleeding in cirrhotic patients are the severity of liver dysfunction, large size of varices and the presence of endoscopic red colour signs but only one-third of patients who have variceal haemorrhage have the above risk factors. Recent interest has been directed at identifying haemodynamic factors that may reflect the pathophysiological changes which lead to variceal bleeding, e.g. it has been confirmed that no bleeding occurs if HVPG falls below 12 mmHg and also a hypothesis has been put forward in which bacterial infection is considered a trigger for bleeding. Pharmacological treatment with beta-blockers is safe, effective and is the standard long-term treatment for the prevention of recurrence of variceal bleeding. Combination of beta-blockers with isosorbide-5-mononitrate needs further testing in randomized controlled trials. The use of haemodynamic targets for reduction in HVPG response needs further study, and surrogate markers of pressure response need evaluation. If endoscopic treatment is chosen, variceal ligation is the modality of choice. The combination of simultaneous variceal ligation and sclerotherapy does not offer any benefit. However, the use of additional sclerotherapy for the complete eradication of small varices after variceal ligation needs to be evaluated. The results of current prospective randomized controlled trials comparing variceal ligation with pharmacological treatment are awaited with great interest. Finally, the use of transjugular intrahepatic portosystemic shunt (TIPS) for the secondary prevention of variceal bleeding is not substantiated by current data, as survival is not improved and because of its worse cost-benefit profile compared to other treatments. In contrast, there still is a role for the selective surgical shunts in the modern management of portal hypertension. The ideal patients should be well compensated cirrhotics, who have had troublesome bleeding - either who have failed at least one other modality of therapy (drugs or ligation), have bled from gastric varices despite medical or endoscopic therapy, or live far from suitable medical services. Recently, ligation has been compared to beta-blockers for primary prophylaxis but so far there is no good evidence to recommend banding for primary prophylaxis, if beta-blockers can be given.
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Terminalia arjuna, an Indian medicinal plant, has been reported to have beneficial effects in patients with ischemic heart disease in a number of small, open studies. The need for a double-blind, randomized, placebo-controlled study with adequate sample size has long been felt. The bark extract (IPC-53) contains acids (arjunic acid, terminic acid), glycosides (arjunetin arjunosides I-IV), strong antioxidants (flavones, tannins, oligomeric proanthocyanidins), minerals. etc. and exhibits antifailure and anti-ischemic properties.
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To assess the impact of long-term oral nitrate therapy on clinical outcome following percutaneous coronary intervention (PCI) in patients with type II diabetes.
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The action of isorsorbide-5-mononitrate (IS-5-MN) infusion (range 6.0 to 10.0 mg/hour) was studied in 24 patients with and without acute heart failure (hemodynamic subsets I to IV) during acute myocardial infarction. Hemodynamic measurements were performed by right-sided cardiac catheterization. Intravenous IS-5-MN demonstrated significant hemodynamic effects compared with baseline values. In subsets I and II, a decrease in pulmonary wedge pressure (PWP) and in cardiac index (CI), without significant changes in heart rate, mean arterial pressure or systemic vascular resistance index were demonstrated. In subsets III and IV, a major increase in CI and a decrease in systemic vascular resistance index, as well as a decrease in PWP were found. Again no changes occurred in mean arterial pressure and heart rate. The dosage was similar in subsets I to IV (8.0, 7.9, 7.8 and 7.3 mg/hour); thus, the differences in the responses could not be attributed to dosage. It appears that several different patterns of hemodynamic IS-5-MN action exist, assuming that IS-5-MN operates on preload and afterload levels. The action of IS-5-MN mechanisms seems to be dependent on an initial hemodynamic subset. No patient had any deleterious hemodynamic effects. A decrease in CI in subsets I and II was not of clinical importance with these dosages. No nitrate tolerance during 9.0 hours of continuous therapy appeared.(ABSTRACT TRUNCATED AT 250 WORDS)
The objective of this study was to evaluate cervix length and the presence of cervical gland area (CGA) in ultrasounds performed before and after the administration of vaginal isosorbide mononitrate (IMN) for cervical ripening.
In a double-blind, randomized cross-over study the antianginal efficacy and tolerability of Elantan Long (50 mg sustained-release IS-5-MN) were compared with a 80-mg sustained-release (s.r.) IS-5-MN formulation. 28 patients were enrolled in the study, which consisted of a 3-day washout period on placebo, an active treatment of 14 days (cross-over after 7 days) and a final 3-day withdrawal period on placebo. Ergometric exercise tests with simultaneous ECG monitoring were carried out 2 and 10 h post administration (p.a.) on the last days of each period. Under 50 mg s.r. IS-5-MN the mean ST- segment depression under comparable load was reduced by 67% 2 h p.a. and by 70% 10 h p.a. The reduction under the 80 mg IS-5-MN form was about 76% 2 h p.a. and 78% 10 h p.a. Maximum workload, working capacity, duration of exercise, time to angina pectoris and time to ST-segment depression greater than 0.1 mV were markedly increased under therapy with each dosage. Comparisons between the medications revealed significant differences only in time to ST-segment depression greater than 0.1 mV and in ST-segment depression under maximum workload at 10 h p.a. which were increased more by the higher dosage. The incidence of anginal attacks decreased by almost 80% in the patients under both treatments. Ten patients under each dosage were completely freed from attacks. Adverse drug reactions occurred in 14 patients, 10 times under 80 mg s.r. IS-5-MN, 5 times under Elantan Long and twice under placebo.(ABSTRACT TRUNCATED AT 250 WORDS)
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Clinical and device evaluation of efficacy of new dosage forms of isosorbide-5-mononitrate (ISMN) in patients with angina of effort of functional class (FC) II-III in 1-3 month treatment.
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Clinical findings and invasive monitoring showed signs of a hyperdynamic hemodynamic cardiovascular failure caused by toxic vasodilatation.
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In the prevention of variceal rebleeding, beta-blockers +/- nitrates are as effective as endoscopic banding.
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It is concluded that intermittent administration of nitrates does not cause rebound angina and is therefore safe. A randomized controlled trial is needed to find the long-term effect on cardiac events.
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We investigated the suitability of BMDP and SAS as an integrated tool for the evaluation of regional blood flow data obtained from the radioactive microsphere technique. Both packages were applied to a recent study on muscle blood flow with a 3-factorial design. The organization of data and files, the strategy of data reduction, and the evaluation by means of statistical and graphical techniques are shown. The method may be applied to any microsphere study design. A considerable amount of time can be saved and data integrity may be improved. The statistical quality of the results may benefit from the broad spectrum of statistical tests available.
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ISMN b.i.d. eccentrically has an antianginal effect throughout most of the day, peaking at 2 h. This effect is sustained during chronic therapy, without tolerance or rebound.
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