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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Increased levels of cyclic guanosine monophosphate, cyclo-oxygenase 2, prostaglandin F(2 alpha), and prostaglandin E(2) were found in samples that were exposed to isosorbide 5-mononitrate compared with control samples. Electron microscopy revealed stromal edema and collagen disorganization after isosorbide 5-mononitrate treatment.
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The patient developed a Brugada-like electrocardiographic pattern twice under the influence of bupivacaine. The first occurrence was accompanied by ventricular tachycardia (VT) which subsided after withdrawal of the anesthetic. The VT was also observed during co-administration of diltiazem and isosorbide-5-mononitrate, agents thought to facilitate ST segment elevation in the Brugada syndrome. Genetic analysis revealed a missense mutation in the alpha subunit of the cardiac sodium channel, SCN5A. Biophysical analysis by whole-cell patch-clamping revealed a reduction in sodium current as a result of the mutation. The study of bupivacaine in the wedge model revealed use-dependent changes in conduction, heterogeneous loss of the action potential dome in RV epicardium and phase 2 re-entry when the preparations were pretreated with low concentrations of the calcium channel blocker verapamil.
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The addition of drug therapy to EVL improves the efficacy of EVL alone. However, the addition of EVL to β-blockers and ISMN achieves a non-significant decrease of rebleeding with no effect on mortality. Although combination therapy with EVL plus β-blockers ± ISMN is adequate to prevent rebleeding, β-blockers + ISMN alone may be a valid alternative.
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These results suggest that the impairment of endothelium-dependent vasorelaxation induced by atherosclerosis is dependent on gender. This may be due to a greater degradation of extracellular NO in the vessel wall of males.
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Thirty episodes of first upper bleeding occurred; 16 were in the Is-5-Mn group. Actuarial probability of bleeding did not differ between the two groups. Endoscopic variceal red signs were the only independent predictors of early bleeding. Of the 52 patients who died, 28 were in the Is-5-Mn group. The likelihood of death was greater among patients assigned to Is-5-Mn than to Pro, but only in patients older than 50 years (72% vs. 48% at 6 years; P = 0.006). Child-Pugh score, bleeding, age, and assignment to Is-5-Mn were independent predictors of death. The likelihood of death without bleeding was also higher (P = 0.05) in the Is-5-Mn group.
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Cardiology outpatient clinic of a university-affiliated municipal hospital.
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Safety has been assessed in a total of 1680 subjects who were treated with nicorandil, with 458 patient years of exposure to treatment. Adverse events usually occurred early in the course of treatment. After 30 days of treatment, fewer than 10% of patients reported adverse events. At the recommended doses, the main side effects were limited to headaches. Nearly all episodes of headache were experienced during the first days of nicorandil treatment and were responsible for most of the study withdrawals because of clinical non-acceptability. The incidence can be diminished by a progressive titration. In comparative trials with anti-anginal agents, such as propranolol, diltiazem, nifedipine, ISDN and isosorbide 5 mononitrate, the overall incidence of adverse events was not significantly different between nicorandil and the reference drug. Side-effect distribution was comparable between nicorandil (32%) and diltiazem (30%). Nicorandil can be safely combined with other anti-anginal drugs. Furthermore, due to its favourable pharmacokinetics, nicorandil is less likely to have interactions when combined with another therapeutic agent. Nearly one-third of the patients enrolled in the nicorandil clinical programme were 65 years old or older. Age-specific side-effects were not identified, and overall, the incidence of the most frequent adverse events in the elderly was similar. There is no evidence that nicorandil induces proarrhythmia, exacerbation of myocardial ischaemia or abrupt withdrawal syndrome. With the progressive titration scheme, no symptomatic decrease in blood pressure was recorded when nicorandil was administered in the range of 10-80 mg.day-1. Heart rate was not significantly affected in the same dose range.(ABSTRACT TRUNCATED AT 250 WORDS)
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In an open-label self-controlled study of 1,350 patients with stable angina pectoris (SAP), we previously demonstrated that 50 mg of isosorbide mononitrate (ISMN) slow release formulation once daily not only provided a better antianginal effect but also a better quality of life (QOL) than did the daily administration of multiple small doses of the compound. It is unknown whether certain patient characteristics contribute to this benefit. The objective of this article was to determine what independent factors contribute to this benefit. Multiple linear regression analysis was performed on the data from these 1,350 patients. Quality of life was assessed by the Marquis QOL-questionnaire for patients with angina and included the domains of immobility, pain, and psychological distress. For the purpose of this study, overall QOL was calculated as the pooled sums of the domain scores and expressed as mean scores on an ordinal scale of 10. Age did not influence the beneficial effect of nitrate therapy on QOL. Neither did gender, rhythmic disturbances, peripheral artery disease, or the concomitant use of calcium channel blockers or beta blockers. New York Heart Association (NYHA) angina classification was an independent variable: patients with a NYHA class I or II benefited less than did patients with NYHA III or IV (p = 0.02). Obese patients as well as hypertensive patients benefited less (p = 0.04 and 0.02), and smokers tended to benefit less also (p = 0.08). In contrast, hypercholesterolemia and diabetes mellitus improved the beneficial effect of nitrates on QOL (p = 0.03 and 0.05). The authors conclude that patients with coronary artery disease (CAD) and concomitant diabetes mellitus or hypercholesterolemia, a category particularly prone to early endothelial dysfunction and thus dysfunctional endogenous nitric oxide (NO) production, may benefit more from NO-donor therapy than patients without such concomitant conditions.
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.
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.
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Nineteen patients with ischemic heart disease were studied to determine plasma levels of isosorbide dinitrate (ISDN) and its metabolites, isosorbide-2-mononitrate (2-ISMN) and isosorbide-5-mononitrate (5-ISMN) for 6 hrs during intravenous administration of ISDN, using gas chromatography. Differences in plasma levels of these substances were also evaluated in patients with or without preanesthetic medication of ISDN. These patients ranging in ages from 42 to 80 years were administered ISDN intravenously at a rate of 1 micrograms.kg-1 x min-1 during anesthesia and surgery. Preanesthetic administration of ISDN consisted of transdermal application of 40 mg dose. Surgery included gastrectomy, pneumonectomy, extended cholecystectomy, radical mastectomy and so on under either enflurane anesthesia or neuroleptanesthesia. Plasma ISDN levels increased and reached a plateau 3 hrs after the start of intravenous infusion of ISDN in patients of both groups. Plasma 2-ISMN levels increased gradually and reached a plateau 5 hrs after the commencement of intravenous administration of ISDN in patients of both groups. Plasma 5-ISMN levels increased gradually reaching the peak 6 hrs after the start of intravenous infusion of ISDN in both groups. Plasma ISDN, 2-ISMN and 5-ISMN levels were slightly higher in patients who received preanesthetic ISDN than in those who did not receive preanesthetic ISDN. However, there were no statistical differences in plasma ISDN or 2-ISMN levels between the groups except prior to the infusion. On the contrary, plasma 5-ISMN levels were significantly higher in patients who received preanesthetic ISDN than in those who did not receive preanesthetic ISDN for 3 hrs after the start of the infusion.
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Nitroglycerin and isosorbide dinitrate (ISDN), the most commonly used nitrate vasodilators, have been shown to possess antiplatelet properties. It has also been shown, interestingly, that their inhibition of aggregation (mostly upon ADP and adrenaline) occurs in vivo at concentrations 1-2 log orders lower than in vitro, and in the full therapeutic range. Many different hypotheses may explain such an in vivo/in vitro difference: 1) that nitrates induce prostacyclin synthesis; 2) that they synergize prostacyclin; 3) that they give rise to more active in vivo metabolites; 4) that some other requirement for their action, such as the availability of reducing thiols, may be a limiting factor in the in vitro setting. The discrimination among such hypotheses should contribute new insights into nitrate action at the platelet level. On the basis of experiments on cultured endothelial cells and vascular fragments, we had previously concluded against prostacyclin induction by nitrates. On the other hand, ISDN may decrease the IC50 for prostacyclin in aggregation by suprathreshold doses of various aggregating agents, and therefore, be synergistic with this endogenous antiplatelet substance. Compared to ISDN, the two longer-lived metabolites isosorbide-2- and isosorbide-5-mononitrates (IS-2-MN, IS-5-MN) appear remarkably different in terms of antiplatelet potency in vitro (minimum effective concentrations 10(-7)-10(-6)M for IS-2-MN, 10(-4)M for IS-5-MN, for ADP-and adrenaline-induced aggregation and thromboxane (TX) B2 production).(ABSTRACT TRUNCATED AT 250 WORDS)
imdur dose conversion
A total of 31 men aged 35 years or older with coronary artery disease (at least 50% narrowing of the left main stem or at least 70% narrowing of any other coronary artery) and erectile dysfunction (receiving medication for erectile dysfunction or scoring less than 26 out of a maximum score of 30 on the erectile function domain questions of International Index of Erectile Function) were randomized to sildenafil 100 mg (n = 10), ISMN 40 mg (n = 11), or placebo (n = 10) in this single-dose multicenter study.
Labor induction in the presence of unfavorable cervix is a common indication for the use of prostaglandins. However, in the last years, there has been a considerable interest in the use of nitrous oxide donors for cervical ripening and labor induction.
No significant changes in ON flow, PP, IOP, or BPm were observed following placebo. Following ISMO, ON flow increased from baseline by 19.8% (SEM 9.3%) at 1 hour (paired t test, p = 0.058) and by 33.1% (7.5%) at 3 hours (p = 0.007). Compared with the changes following placebo, statistically significant increases in ON flow were observed both at 1 (p = 0.050) and 3 hours (p = 0.041) after ISMO treatment. Compared with placebo, PP decreased significantly 1 hour after ISMO dosing (p = 0.039), mainly as a function of reduced BPm. A significant inverse correlation (R = -0.618; p = 0.032) was observed between the percentage changes in PP and ON flow 1 hour following ISMO administration, but not after placebo. No significant change in foveal Ch flow was documented.
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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.
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Carvedilol may be more effective in decreasing HVPG than propranolol or nebivolol and it may be as effective as EVL or nadolol plus ISMN in preventing variceal bleeding. However, the overall quality of evidence is low. Further large-scale randomised studies are required before we can make firm conclusions.
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Epidemiological studies suggest that women with heart failure differ from men with heart failure in that their survival is better. Therapeutic trials have not clearly demonstrated a survival benefit for women. This study was to determine the tolerance for high doses of angiotensin-converting enzyme (ACE) inhibitor-nitrates in women versus men and to compare their symptomatic response, exercise tolerance, and ventricular functional improvement over 1 year. Eighty-eight sequential patients with heart failure, 54 men and 34 women with left ventricular ejection fraction < or = 35%, were prospectively followed for 1 year. For all patients, ACE inhibitor-nitrate therapy was intensified. Each patient had three 6-monthly echocardiograms at baseline, at 6 months, and at 1 year, and metabolic stress testing. Patients were 57.3 +/- 12.3 years old, with New York Heart Association (NYHA) class severity 2.6 +/- 1.0. Lisinopril dosages were raised from 14 +/- 14 mg/day to 57 +/- 26 mg/day, isosorbide mononitrate from 15 +/- 27 mg/day to 126 +/- 72 mg/day, and carvedilol (n = 34) to 17 +/- 16 mg/day. Women and men were epidemiologically comparable, with similar baseline echocardiographic parameters (left ventricular ejection fraction 19% +/- 7% versus 17% +/- 6%, respectively). Both tolerated up-titration in medical therapy. Final 12-month ejection fractions were equivalent for women and men at 34% +/- 17% and 34% +/- 13%, respectively, with similar improvements in left ventricular diameters. At 1 year, women had higher resting heart rates and remained more symptomatic with lower exercise capacity. However, the relative changes in NYHA status and aerobic capacity were similar for women and men. Thus, both women and men tolerated uptitrated ACE inhibitor-nitrate medical therapy, with comparable reversal of heart failure remodeling. Although women continued to be more symptomatic than men, relative improvements in symptomatic status, in exercise capacity, and in hospitalization rate were equivalent.
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Our aim was to examine the efficacy, safety, and acceptability of isosorbide mononitrate for cervical ripening and labor induction in women in an outpatient setting.
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Isosorbide-5-mononitrate (IS-5MN) is an active metabolite of isosorbide dinitrate, but unlike its parent compound, is nearly 100% bioavailable after oral administration. Once-a-day therapy with a slow-release formulation of IS-5MN is used widely in Europe for 24-hour prophylaxis of angina pectoris. In a randomized, crossover, double-blind, placebo-controlled study, the duration of effects of 50 and 100 mg of slow-release IS-5MN were evaluated after the first dose and after once-a-day therapy for 1 week in 9 patients with stable angina pectoris. Compared with placebo values, standing blood pressure decreased (p less than 0.001) and exercise time to the onset of angina and total exercise duration increased (p less than 0.008 and p less than 0.003) at 4 hours, but not at 20 or 24 hours after first dose of 50 and 100 mg of slow-release IS-5MN. After once-a-day therapy for 1 week, no improvement in exercise duration or reduction in ST-segment depression was seen after 50 or 100 mg of slow-release IS-5MN at 4, 20 or 24 hours despite high plasma IS-5MN concentrations. Thus, despite therapeutic plasma concentrations, 50 and 100 mg of slow-release IS-5MN did not exert antianginal or anti-ischemic effects at 20 and 24 hours after the first dose and at 4, 20 and 24 hours after sustained once-a-day therapy for 1 week.
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