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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To assess the acute and chronic effects of propranolol, and the effect of the acute addition of isosorbide-5-mononitrate, on splanchnic circulation.
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Asymmetric dosage regimens of isosorbide mononitrate provide better antianginal efficacy and quality of life in patients with stable angina pectoris than the daily administration of multiple small doses of the compound. It is not known whether certain patient characteristics contribute to this improved benefit.
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Early treatment with converting enzyme inhibitors and nitrates in acute myocardial infarction may limit infarct expansion and prevent left ventricular dilation.
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Isosorbide-5-mononitrate (ISMO) has been shown to be effective in reducing the risk of variceal bleeding in patients with cirrhosis. However, recent studies have suggested that this drug compromises renal function. The present study was conducted to assess the acute and chronic effects of ISMO on effective renal plasma flow (ERPF) and the renin-aldosterone profile in cirrhotic patients.
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12 patients with coronary heart disease were studied to see whether high doses of isosorbide dinitrate (ISDN, Corovliss) or isosorbide 5-mononitrate (IS-5-MN, Ismo) increase the erythrocyte methemoglobin production in an acute experiment and after 4 days of medication. The patients were divided into two groups. Group 1 (6 patients) was given a single dose of 80 mg ISDN on the morning of day 1 and Group 2 (6 patients) was given 80 mg IS-5-MN as a single oral dose. Under the influence of the IS-5-MN no change was observed from the initial methemoglobin (met-Hb) value (0.81% of the total Hb) at measurements performed 1 and 2 h after the administration of the drug. In Group 1 (ISDN) the initial met-Hb value was 0.58% of the total Hb, a slight increase to 0.70% being observed after 1 h and to 0.77% after 2 h (p less than 0.05). The patients were then treated as follows for a further 4 days: Group 1 480 mg ISDN/d, Group 2 480 mg IS-5-MN/d. On day 5 the initial met-Hb values in both groups were unchanged compared to day 1. The patients were then given first 80 mg ISDN (Group 1) or 80 mg IS-5-MN (Group 2) and 4 h later a single dose of 160 mg of the appropriate substance. In Group 2 (IS-5-MN) the met-Hb content remained unaffected. In Group 1 a slight increase of the met-Hb to 0.79% occurred 1 h after 80 mg ISDN and to 0.9% after 2 h (p less than 0.05). The dose of 160 mg ISDN gave rise to a further slight increase to 1.00% (after 1 h) and 1.13% (after 2 h) (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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It is clearly established that beta-blockers decrease the risk of a first variceal bleeding in cirrhosis. We have recently shown that the addition of isosorbide mononitrate to nadolol decreases the rate of variceal bleeding in patients with cirrhosis and varices, compared with nadolol alone, after a median follow-up of 30 months. It is not established if the long-term treatment with the combination continues to be beneficial. Therefore, we assessed the long-term effect of this combination on first variceal bleeding, complications, and death. One hundred forty-six cirrhotic patients with esophageal varices included in a previously published multicenter, randomized study comparing nadolol (40-160 mg/d) with the combination nadolol plus isosorbide mononitrate (10-20 mg 3 times per day) were followed up for up to 7 years (median follow-up, 55 months). The primary end-point was variceal bleeding of any severity. Twenty-four patients (16 in the nadolol group, and 8 in the combination group) experienced variceal bleeding (log rank test, P =.02). Cumulative risk of bleeding was 29% and 12%, respectively (95% CI for the difference, 1%-23%). Two and 4 patients, respectively, had bleeding from portal hypertensive gastropathy (log rank test, P =.20). Thirty and 25 patients, respectively, died during follow-up (log rank test, P =.13). Twelve and 10 patients, respectively, had de novo occurrence of ascites during follow-up (log rank test, P =.29). In conclusion, nadolol plus isosorbide mononitrate is significantly more effective than nadolol alone in the long-term use. Side effects are few, and no deleterious effects on ascites occurrence or on survival occur after long-term use of this combination.
Bioconversion of glyceryl trinitrate (GTN) into nitric oxide (NO) by aldehyde dehydrogenase-2 (ALDH-2) is a crucial mechanism which drives vasodilatory and antiplatelet effect of organic nitrates in vitro and in vivo. Oxidative stress generated by overproduction of free radical species, mostly superoxide anions and NO-derived peroxynitrite, has been suggested to play a pivotal role in the development of nitrate tolerance, though the mechanism still remains unclear. Here we studied the free radical-dependent impairment of ALDH-2 in platelets as well as vascular tissues undergoing organic nitrate ester tolerance and potential benefit when using the selective peroxynitrite decomposition catalyst Mn(III) tetrakis (4-Benzoic acid) porphyrin (MnTBAP). Washed human platelets were made tolerant to nitrates via incubation with GTN for 4h. This was expressed by attenuation of platelet aggregation induced by thrombin (40U/mL), an effect accompanied by GTN-related induction of cGMP levels in platelets undergoing thrombin-induced aggregation. Both effects were associated to attenuated GTN-induced nitrite formation in platelets supernatants and to prominent nitration of ALDH-2, the GTN to NO metabolizing enzyme, suggesting that GTN tolerance was associated to reduced NO formation via impairment of ALDH-2. These effects were all antagonized by co-incubation of platelets with MnTBAP, which restored GTN-induced responses in tolerant platelets. Comparable effect was found under in in vivo settings. Indeed, MnTBAP (10mg/kg, i.p.) significantly restored the hypotensive effect of bolus injection of GTN in rats made tolerants to organic nitrates via chronic administration of isosorbide-5-mononitrate (IS-5-MN), thus confirming the role of peroxynitrite overproduction in the development of tolerance to vascular responses induced by organic nitrates. In conclusion, oxidative stress subsequent to prolonged use of organic nitrates, which occurs via nitration of ALDH-2, represents a key event in GTN tolerance, an effect counteracted both in vitro and in vivo by novel peroxynitrite decomposition catalyst.
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Although nitrates were introduced more than 100 years ago and have been used for the treatment of angina pectoris, there are still some open questions concerning the mechanism of their action on myocardial ischemia. There are also insufficient data regarding the influence of any anti-ischemic medication on the results of myocardial perfusion scintigraphy.
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To investigate whether isosorbide-5-mononitrate (Is-5-Mn) given with propranolol reduces hepatic portal pressure more than does propranolol alone in patients with cirrhosis.
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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.
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A comparative, randomised, 12-week (two periods of six weeks) cross-over study including 150 patients (mean age: 63.4 years) suffering from stable but symptomatic (a minimum of three attacks per week) angina pectoris was performed in order to compare the effect on quality of life of two discontinuous nitrate treatments: transdermal 10 mg nitroglycerine patch (12 hours) and long-acting oral 40 mg isosorbide-5-mononitrate (once a day). The efficacy and safety were also compared. The two treatments equally and significantly improved patients' quality of life. The number of attacks and sublingual nitrate consumption significantly decreased under treatment. Attack severity was lower under nitroglycerine than isosorbide-5-mononitrate treatment. Finally, even though nitroglycerine more frequently induced headache than did isosorbide-5-mononitrate (13 cases versus 8), patients, and in particular those having received nitroglycerine treatment in the second period of the study, preferred the transdermal nitroglycerine treatment. In conclusion, results did not show any relevant difference in terms of efficacy or tolerability between the two treatments. Nevertheless, the facility of use and the feeling of protection were better under transdermal nitroglycerine patch than oral isosorbide-5-mononitrate treatment.
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In patients with compensated or slightly decompensated liver cirrhosis 5-isosorbide mononitrate, propranolol or the association of both did not produce detectable worsening of subclinical hepatic encephalopathy or renal function.
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In the whole series, no significant correlation was found between hepatic venous pressure gradient and duplex Doppler parameters, but, when the 12 patients with a patent para-umbilical vein were excluded, significant linear correlations were found between hepatic venous pressure gradient and portal blood velocity (r=-0.39; p=0.05) or congestion index (r=0.37; p=0.05). Considering together the changes induced by nadolol and nadolol plus isosorbide-5-mononitrate, no correlation was apparent between changes in duplex Doppler parameters and in hepatic venous pressure gradient. Agreement between hepatic venous pressure gradient and duplex Doppler parameters in defining good and poor responders was insufficient.
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In some but not all arterial beds, smooth muscle cell calcium-activated K+ channels (KCa channels) play a central role in the mediation of the vasodilator response to nitric oxide (NO) and other nitrates. We investigated the effect of nitrates on KCa channels in the relaxation of human coronary arteries by means of isometric contraction experiments in arterial rings. We also measured whole-cell currents in freshly isolated human coronary artery vascular smooth muscle cells via the patch-clamp technique. Sodium nitroprusside, diethylamine-nitric oxide complex sodium salt and isosorbide mononitratre completely relaxed rings preconstricted with 5 microM serotonin and produced dose-dependent relaxations of 5 microM serotonin-preconstricted human rings. The relaxations were inhibited by 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-oxyl 3-oxide (10 microM), which neutralizes nitric oxide. The KCa channel blockers iberiotoxin (100 nM) and tetraethylammonium ions (1 mM) significantly inhibited SNP-induced relaxations of human coronary arteries. Moreover, in the patch-clamp experiments, SNP (1 microM) stimulated KCa currents and spontaneous transient outward K+ currents carried by Ca spark activated KCa channels. The SNP-induced (1 microM) KCa current was strongly inhibited by iberiotoxin (100 nM). These data show that activation of KCa channels in smooth muscle cells contributes to the vasodilating actions of nitrates and nitric oxide in human coronary arteries. This finding may have unique clinical significance for the development of antianginal and antihypertensive drugs that selectively target K+ channels and Ca sparks.
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Organic nitrate vasodilators (ORN) exert their pharmacologic effects through the metabolic release of nitric oxide (NO). Mitochondrial aldehyde dehydrogenase (ALDH2) is the principal enzyme responsible for NO liberation from nitroglycerin (NTG), but lacks activity towards other ORN. Cytosolic aldehyde dehydrogenase (ALDH1a1) can produce NO from NTG, but its activity towards other ORN is unknown. Using purified enzymes, we showed that both isoforms could liberate NO from NTG, isosorbide dinitrate (ISDN), and nicrorandil, while only ALDH1a1 metabolized isosorbide-2-mononitrate and isosorbide-5-mononitrate (IS-5-MN). Following a 10-min incubation with purified enzyme, 0.1 mM NTG and 1 mM ISDN potently inactivated ALDH1a1 (to 21.9% ± 11.1% and 0.44% ± 1.04% of control activity, respectively) and ALDH2 (no activity remaining and 4.57% ± 7.92% of control activity, respectively), while 1 mM IS-5-MN exerted only modest inactivation of ALDH1a1 (reduced to 89% ± 4.3% of control). Cytosolic ALDH in hepatic homogenates incubated at the vascular EC(50) concentrations of ORN was inactivated by NTG (to 45.1% ± 8.1% of control activity) while mitochondrial ALDH was inactivated by NTG and nicorandil (to 68.2% ± 10.0% and 78.7% ± 19.8% of control, respectively). Via site-directed mutagenesis, the active sites of ORN metabolism of ALDH2 (Cys-319) and ALDH1a1 (Cys-303) were found to be identical to those responsible for their dehydrogenase activity. Cysteine-302 of ALDH1a1 and glutamate-504 of ALDH2 were found to modulate the rate of ORN metabolism. These studies provide further characterization of the substrate selectivity, inactivation, and active sites of ALDH2 and ALDH1a1 toward ORN.
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The patients were randomly assigned to three groups: 0.1% ISMN gel (21 patients), 0.1% GTN gel (21 patients) and a placebo group (ten patients). The ethic committee of our hospital approved the protocol and informed consent was obtained from all participants. All patients underwent clinical examination, visual inspection of the fissure and anal manometry prior to and after therapy.
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To compare the efficacy and safety of vaginal applications of three different principles of cervical priming prior to first trimester curettage, isosorbide mononitrate (ISMN), misoprostol and Dilapan-S, a hygroscopical cervical dilator.
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Pharmacokinetics of 20 mg isosorbide-5-mononitrate (IS-5-MN) after single and multiple administration of two different tablet formulations were investigated in twelve healthy human subjects using an open, randomized, two-way crossover experimental design. Pentacard 20 mg tablets were compared with Ismo 20 mg tablets. After single-dose administration, both preparations caused a rapid increase in IS-5-MN plasma levels with the peak plasma concentration occurring between 0.5 and 1.5 h. For both formulations, the mean plasma half-life was found to be approximately 5 h after a single dose. In steady state during multiple dosing (t.i.d. at 8 h dosing intervals), a reduced elimination rate was observed. In line with this observation, the area under the plasma concentration-time curve (AUC) for one 8 h dosing interval during multiple dosing was higher than the extrapolated AUC after a single dose. Based on statistical evaluation of the various relevant pharmacokinetic parameters calculated from the plasma concentrations occurring after single and multiple dosing, the tablet formulations are judged to be bioequivalent.
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Over a 6-year period, 172 patients with cirrhosis, grade II or III esophageal varices that had never bled, were recruited; 44 into VBL, 66 into PPL, and 62 into ISMN. Baseline patient characteristics: age, 55 +/- 11 years; Child-Pugh score, 8 +/- 2; 65% alcohol-induced cirrhosis; follow-up period, 19.7 +/- 17.6 months (range, 0.13-72.1 months), were comparable in the 3 groups.
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1. The aim of the present study was to evaluate the effect of preventive and curative isosorbide-5-mononitrate (Is-5-Mn) treatment on the development of hypertension, cGMP content, thromboxane (TX) A(2)/prostaglandin (PG) I2 balance, the peripheral serotonergic system, platelet activation, lipid peroxidation and plasma lipids in cyclosporine A (CsA)-induced hypertensive rats. 2. Control, CsA (5 mg/kg per day) and Is-5-Mn (150 mg/kg per day, b.i.d.) rat groups were treated orally over a period of 7 weeks. The preventive Is-5-Mn group (Is-5-Mn + CsA) was first treated for 2 weeks with Is-5-Mn, followed by 7 weeks with both drugs; the curative Is-5-Mn group (CsA + Is-5-Mn) was treated for a period of 7 weeks with CsA and with both drugs for an additional 5 weeks. The control group received oral vehicle. 3. Whereas in the group undergoing preventive treatment the CsA-induced increase in blood pressure (BP), compared with the control group, was avoided, in the group undergoing curative treatment, the increase in BP was even higher. The decreased arterial cGMP content in the CsA group was prevented and reverted when Is-Mn was administered either preventatively or curatively with CsA. Platelet TXA2 production, although unaffected in the Is-5-Mn + CsA group, was significantly higher in the CsA + Is-5-Mn group compared with the group receiving CsA alone. Furthermore, plasma TXA2 was reduced following preventive Is-5-Mn treatment, but was worsened in the group undergoing curative therapy. Aortic PGI2 synthesis was identical in all groups. Consequently, the TXA2/PGI2 ratio was only altered in the CsA + Is-5-Mn group, demonstrating a markedly higher value. In both groups treated simultaneously with CsA and Is-5-Mn, a higher platelet 5-hydroxytryptamine (5-HT) content was obtained compared with CsA treatment alone, but only preventive treatment with Is-5-Mn resulted in a significant reduction in plasma 5-HT. Changes in ADP and collagen-induced platelet aggregation paralleled those of plasma 5-HT and TXA2: the hyperaggregation profile of the CsA group, although partially prevented, was not reverted by simultaneous treatment with Is-5-Mn and CsA. Lipid peroxidation and lipid profile values also worsened in the CsA + Is-5-Mn group compared with the group administered CsA alone. 4. In conclusion, the beneficial effects of concomitant Is-5-Mn and CsA treatment were demonstrated when Is-5-Mn was administered preventatively because not only was arterial hypertension prevented, but platelet aggregation and plasma TXA2 and 5-HT levels were also reduced. In contrast, following curative treatment, the BP, platelet/vascular vasoconstrictor balance, lipid peroxidation and plasma lipids were aggravated, recommending a judicious evaluation of the impact of nitrate therapy throughout the period of its administration.
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During the night/morning hours, healthy controls demonstrated faster HF max. velocity (P=0.002) and higher HF gradient (P=0.011) than angina patients. Metoprolol and IS-5-MN increased the HF gradient (P=0.008 and P=0.003, respectively), and metoprolol tended to increase the max. velocity (P=0.02). Metoprolol substantially decreased the LF/HF gradient (P=0.001), velocity (P=0.008) and max. velocity (P=0.0001).
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Nitric oxide (NO) donors are capable of ripening the human cervix during pregnancy. The purpose of this study was to examine how NO donors may be involved in this process. Cervical biopsies were obtained from pregnant women randomized to receive isosorbide mononitrate (n = 10) or no treatment (n = 10) prior to suction termination. Enzyme-linked immunosorbent assays (ELISA) were performed on culture supernatant for interleukin (IL)-1, IL-6, IL-8, IL-10, IL-15, tumour necrosis factor-alpha, monocyte chemoattractant protein-1 and prostaglandin metabolites. Immunohistochemistry was performed to localize these cytokines, cyclooxygenase (COX)-1, COX-2 and prostaglandin dehydrogenase in cervical tissue and reverse transcription-polymerase chain reaction (RT-PCR) to identify COX-1 and COX-2 expression. Biopsies treated with the NO donor isosorbide mononitrate (IMN) produced significantly greater amounts of prostaglandin F(2alpha) in culture and lower amounts of thromboxane B(2) than controls (572.8 versus 34.9 pg/ml, P < 0.05; 53.3 pg/ml versus 530.9 pg/ml, P < 0.01 respectively). The release of other prostaglandins and of cytokines was not affected by treatment with NO. Inflammatory mediators were localized to cervical tissue and COX-1 and COX-2 expression was confirmed by RT-PCR. In conclusion, the mechanism of NO donor-induced cervical ripening during pregnancy may be mediated in part via increased prostaglandin F(2alpha) synthesis.
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