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PubMed1981

Pharmacokinetics of isosorbide dinitrate in rhesus monkey, cynomolgus monkey, and baboon.

At 2 min after intravenous injection of isosorbide dinitrate (1 mg/kg), mean plasma drug concentrations were 565 +/- 66 (SD), 586 +/- 43, and 1572 +/- 253 ng/ml in the rhesus monkey, cynomolgus monkey, and baboon, respectively. Following a relatively short distribution phase, mean plasma concentrations declined with half-lives of 62, 23, and 24 min in these three species, respectively. The time course of plasma concentrations could be described by a two-compartment open model, although a one-compartment open model was adequate for obtaining some pharmacokinetic parameters. Statistically significant differences among the species were observed in areas under the plasma concentration-time curves, plasma half-lives, and volumes of distribution. The pharmacokinetics kinetics of isosorbide dinitrate in baboons most closely resembled those in humans.

Animals↗
PubMed1982

[Pharmacokinetics of isosorbide dinitrate administered by intravenous infusion to hypertensive patients (author's transl)].

The pharmacokinetics of intravenous isosorbide dinitrate was investigated in 11 patients with labile hypertension and with normal renal and hepatic functions. The mode of administration (constant rate infusion without loading dose) was chosen in order to minimize side-effects and to approximate clinical conditions. Isosorbide dinitrate levels were measured by electron-capture gas chromatography. The volume of distribution during steady state (Vd beta = 318 +/- 117 I) and the elimination half-life (t1/2 beta = 64.8 +/- 30.5 min) were similar to those found after perlingual and oral administration. Systemic clearance (Cls = 3.80 +/- 1.48 I/min) was high for a drug given intravenously, presumably because of active hepatic extraction, intensive pre-systemic degradation and very active extra-hepatic metabolism. These findings should be compared with the considerable inter-individual variations observed in theoretical plasma concentrations during steady state and with the presence of two pharmacokinetic models (one -- and two -- compartments) in the patients under study. Comparison of the results obtained by the intravenous route with previously published results after perlingual and oral administration indicates the following bioavailability ratios: perlingual/i.v. = 31%, oral/i.v. = 20%, and oral/perlingual = 63%.

Female↗
PubMed1990

Comparison of the effects of a controlled-release formulation of isosorbide-5-mononitrate and conventional isosorbide dinitrate on exercise performance in men with stable angina pectoris.

Thirty-three men with stable exercise-induced angina pectoris entered a randomized, double-blind, crossover study in which controlled-release isosorbide-5-mononitrate 60 mg once daily was compared with conventional isosorbide dinitrate 20 mg 3 times daily. Each drug was given for 2 weeks. Twenty-eight patients completed the study and data on exercise variables are available in 23 patients. Treatment with either drug resulted in significant antianginal effects, when measured 6 hours after a single dose and after 2 weeks of therapy compared with baseline placebo; however, there were significantly fewer signs of myocardial ischemia during treatment with isosorbide-5-mononitrate. There was no evidence of tolerance to either drug treatment but a significant attenuation of resting blood pressure (but not of exercise blood pressure) was observed with both drugs. Headache was the only clinically significant adverse event during therapy and it occurred more frequently in the isosorbide dinitrate treatment group (p less than 0.05 vs placebo); 3 such patients had to withdraw from the study because of headache. Thus, once-daily, controlled-release isosorbide-5-mononitrate appears as effective as conventional isosorbide dinitrate 3 times daily in patients with stable angina pectoris. The once-daily administration is convenient and improves patient compliance.

Angina Pectoris↗
PubMed1997

[Effects of inhalated isosorbide dinitrate on endothelin and nitric oxide and its therapeutic efficacy for experimental guinea-pigs with asthma].

To probe into the correlation between the changes of endothelin and nitric oxide in bronchial alveolar lavage fluid (BALF) and the treatment of inhaling isosorbide dinitrate on experimental guinea pigs with asthma, we divided 25 guinea pigs randomly into three groups (Control group, Asthma group, Isosorbide dinitrate group), and induced some subjects by inhalation of aerosolized ovalbumin as the model of asthma to investigate the endothelin (ET) and nitric oxide (NO) level in BALF as well as the pathological change of the respiratory tract. We found that the level of endothelin and nitric oxide in BALF were all elevated in experimental guinea pigs with asthma, but the degree of increase of NO in BALF was lower than that of ET. The NO and the ET levels in BALF were negative correlation (r = -0.8050, P < 0.01). After having been treated with aerosolized isosorbide dinitrate, the NO level in BALF was significantly elevated and the ET level in BALF was decreased in comparison with the asthma group (P < 0.001, respectively). Moreover, the eosinophile infiltration, exoserosis, and epithalaxia of the respiratory tract of the guinea-pigs were all lightened. The results suggest that inhaled isosoratory dinitrate could be used for treating asthma, and its mechanism may be elevation of NO level and decrease of ET level in BALF.

Administration, Inhalation↗
PubMed1995

Anti-ischemic effects of first and second dose of 20 mg isosorbide dinitrate administered 5 hours apart: attenuation of effects despite rising plasma concentration.

Based on evidence that there may be early tolerance development even within the first daily cycle of treatment, this study was undertaken to evaluate the duration and extent of the antiischemic effects of two 20 mg doses of isosorbide dinitrate as used in a well-established regimen documented to maintain effectiveness during long-term treatment. Ischemia parameters were analyzed at 2 and 4 1/2 hours after the first dose as well as at 2 and 7 hours after the second dose given 5 hours later. The studies were performed in 10 male patients with documented coronary artery disease using bicycle ergometry and a double-blind, randomized, placebo-controlled, crossover protocol. ST-segment depression was reduced by 59% (p < 0.0005) at 2 hours and by 42% (p < 0.01) at 4 1/2 hours after the first tablet and by 38% (p < 0.005) at 2 hours and by 15% (p < 0.05) at 7 hours after the second tablet. Increments in ischemia-free workload capacity amounted to 112% (p < 0.005) and to 41% (p < 0.05) after the first tablet and 68% (p < 0.05) and 38% (p < 0.05) at 2 and 7 hours after the second tablet. At 2 and 4 1/2 hours after the first tablet, plasma concentrations of isosorbide dinitrate were 8.4 and 5.9 ng/ml, and those of isosorbide-5-mononitrate were 166.6 and 130.3 ng/ml. At 2 and 7 hours after the second tablet, the concentrations of isosorbide dinitrate were 9.1 and 5.9 ng/ml, and those of isosorbide-5-mononitrate were 224.5 and 148.1 ng/ml.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1992

Isosorbide dinitrate spray. Attenuation of cardiovascular responses to laryngoscopy and intubation.

We evaluated the efficacy of isosorbide dinitrate buccal spray (Isomack) in attenuating the cardiovascular response to laryngoscopy and tracheal intubation in 60 patients undergoing elective surgery under general anaesthesia. Patients were allocated to one of three groups of 20 patients each. Group 1 patients were administered placebo buccal spray 90 s before induction of anaesthesia. Groups 2 and 3 had isosorbide dinitrate spray 30 and 90 s before induction of anaesthesia. Systolic, diastolic and mean arterial pressures and heart rate were monitored. After the spray, group 3 patients had a significant decrease in systolic arterial pressure (p less than 0.01). At 1 min after intubation, systolic, diastolic and mean arterial pressures showed a significant increase in group 1 patients (24.9 mmHg, 14.2 mmHg and 18.7 mmHg respectively). In contrast, groups 2 and 3 showed a significant decrease in these parameters (p less than 0.01). Although significant tachycardia was present following intubation in all the three groups, the degree of tachycardia was greater in groups 2 and 3 (p less than 0.01).

Adolescent↗
PubMed1983

Intravenous isosorbide dinitrate in acute left ventricular failure--a dose--response study.

The haemodynamic effects of intravenous isosorbide dinitrate (Cedocard) in patients with severe acute left ventricular failure have been assessed using incremental infusion rates from 50 to 800 micrograms min-1. For most patients most of the fall in pulmonary arterial diastolic pressure occurred by 200 micrograms min-1, with little further fall at higher doses. At 200 micrograms min-1 pulmonary arterial diastolic pressure fell from 29 to 23 mgHg (P less than 0.001), there was no significant change in cardiac index (1.9 to 2.0 L min-1 m-2) or heart rate (108 to 108 beats min-1). Despite high doses, no side effects were observed. Intravenous isosorbide dinitrate is effective and safe in the management of acute severe left ventricular failure. In most patients an infusion rate of about 200 micrograms min-1 produces optimal haemodynamic effects.

Adult↗
PubMed1987

Comparison of the inhibitory effects of nicorandil, nitroglycerin and isosorbide dinitrate on vascular smooth muscle of rabbit aorta.

The inhibitory effects of nicorandil, nitroglycerin and isosorbide dinitrate on the contractions induced by 10(-6) M norepinephrine or by 65.4 mM K+ were compared in the vascular smooth muscle of rabbit aorta. These compounds relatively selectively inhibited the contraction induced by norepinephrine. Norepinephrine induced a sustained contraction in the aorta depolarized with high K+ and treated with 10(-6) M verapamil, and this contraction was also inhibited by these compounds. The increase in Ca2+ influx induced by norepinephrine, but not by high K+, was inhibited by the three compounds. The norepinephrine-induced transient contraction, which is due to release of stored Ca2+, was inhibited by these compounds. The inhibitory effects of nicorandil and nitroglycerin on this contraction were attenuated by high-K+ depolarization. Methylene blue (10(-5) M) antagonized and M&B 22948 (10(-5) M) potentiated the inhibitory effects of these compounds. These results suggest that nicorandil, nitroglycerin and isosorbide dinitrate have a similar mechanism of action. These compounds inhibit the norepinephrine-induced sustained contraction possibly by inhibiting the Ca2+ influx through receptor-linked Ca2+ channels, and inhibit the transient contraction by membrane hyperpolarization and also by direct inhibition of Ca2+ release although other mechanism of action may also be involved.

Animals↗
PubMed1983

Transient myopia following isosorbide dinitrate.

A 38-year-old white woman consistently developed transient myopia following the administration of isosorbide dinitrate (Isordil). The myopia was associated with a decreased amplitude of accommodation, a reduction of the AC/A ratio and was eliminated by cycloplegia. Ciliary spasm secondary to the ingestion of this medication is proposed as a possible explanation for the transient myopia. To our knowledge, this case represents the first case of transient myopia following isosorbide dinitrate administration.

Accommodation, Ocular↗
PubMed1992

Vasodilatory response of the coronary arteries after Kawasaki disease: evaluation by intracoronary injection of isosorbide dinitrate.

OBJECTIVE: To determine coronary artery diameter change before and after an intracoronary infusion of isosorbide dinitrate in patients who have had Kawasaki disease, we performed coronary angiography in 188 such patients. PATIENTS AND METHODS: Four patient groups were studied. Groups 1 to 3 consisted of patients with Kawasaki disease: group 1 (the "normal" group; n = 65) had no coronary artery lesions; patients in group 2 had regression to normal of a coronary artery aneurysm after Kawasaki disease and were divided, according to the time since onset, into two subgroups, group 2-a (n = 20) being at an early stage after regression to normal (followed for 1.7 +/- 0.7 years) and group 2-b (n = 34) being at a later stage after regression (followed for 8.7 +/- 2.9 years); and group 3 (the "abnormal" group; n = 25) had persistent coronary artery aneurysm or stenosis or both. Group 4, the control group (n = 44), consisted of patients without Kawasaki disease who had congenital heart disease with normal coronary arteries. The coronary artery diameter change was calculated by the following formula: Percentage of change = (Diameter after infusion - Diameter before infusion)/Diameter before infusion x 100. RESULTS: The percentages of change in the coronary artery diameter after isosorbide dinitrate infusion were 16.2% +/- 13.4% (normal group), 11.3% +/- 7.2% (early-regression group), 7.8% +/- 8.3% (late-regression group), 6.8% +/- 7.8% (abnormal group), and 15.2% +/- 11.8% (control group). In the abnormal group, there was significantly poorer dilation than in the control and normal groups. The late-regression group also had significantly less change in diameter than did the control and normal groups (p < 0.05). CONCLUSIONS: These data suggest (1) that the coronary artery after Kawasaki disease becomes stiff not only in patients with persistent abnormal lesions but also in those with regressed aneurysms and (2) that stiffness of the coronary artery may be a risk factor for atherosclerosis.

Child↗
PubMed1991

Enhanced effectiveness of combined sustained-release forms of isosorbide dinitrate and diltiazem for stable angina pectoris.

In 14 patients with documented coronary artery disease, the extent and duration of acute anti-ischemic, antianginal and hemodynamic effects of monotherapies with 120 mg of sustained-release isosorbide dinitrate and diltiazem were compared; their combined therapy administered once daily in the morning with diltiazem given again in the evening were also compared according to a randomized, double-blind, crossover, placebo-controlled protocol including exercise testing for assessment of ST-segment depression (ST decreases) at an identical work load, exercise capacity and determination of plasma concentrations of both substances. Comparison of individual substances revealed more marked and sustained effects of isosorbide dinitrate (ST decreases at 2 hours, -66%; at 6 hours, -50%; p less than or equal to 0.05 for both), remaining statistically significant up to 12 hours (-24%) than of diltiazem (2 hours, -30%; 6 hours, -16%; p less than 0.05). Combined therapy resulted in increased effects (ST decreases at 2 hours, -80%; 6 hours, -76%; 12 hours, -30%; p less than or equal to 0.05) as opposed to individual substances for a period of up to 12 hours. However, therapeutic coverage over 24 hours could not be demonstrated, even with renewed administration of sustained-release diltiazem in the evening. Plasma concentrations of isosorbide-5-mononitrate were greater than 250 ng/ml for 12 hours on days when isosorbide dinitrate was given, decreasing to less than 100 ng/ml at 24 hours. On days when diltiazem was given, plasma levels greater than 50 ng/ml were detected only at 2 and at 6 hours, and at 24 hours only after a second tablet was given.

Angina Pectoris↗
PubMedDate not supplied

Isosorbide dinitrate or nifedipine: which is preferable in the medical therapy of achalasia?

Oesophageal motor activity was recorded manometrically with a low compliance system in 16 patients with achalasia and a slightly dilated oesophagus. After a basal recording period, nifedipine 20 mg was given sublingually to 9 patients and isosorbide dinitrate 5 mg to another 7 patients. Lower oesophageal sphincter pressure (LESp) and oesophageal body pressure wave amplitude were measured for 60 min after drug administration. Both drugs decreased LESp and pressure wave amplitude, but the effect of isosorbide dinitrate was faster and more intense than that of nifedipine. There was a lower inhibitory effect of nifedipine on the amplitude of pressure waves than on LESp, while isosorbide dinitrate inhibited with a similar intensity both LESp and pressure waves.

Esophageal Achalasia↗
PubMed1982

[Intravenous isosorbide dinitrate in acute cardiac failure (author's transl)].

Isosorbide dinitrate (ISDN) was used by intravenous infusion in 7 patients with acute cardiac failure consecutive to acute (5) or chronic (1) myocardial infarction or to non-obstructive cardiomyopathy (1). Pulmonary artery pressure (PAP), pulmonary capillary pressure (PCP), right atrial pressure (RAP) and cardiac output were measured (PCP), right atrial pressure (RAP) and cardiac output were measured by intracardiac catheterization. The initial dosage of 2.5 mg/hour was increased until PCP was reduced to 15 mmHg or less or until troublesome side-effects developed. Control was achieved in 3 patients with doses of 2.5 to 7 mg/hour and, to a lesser extent, in one patient with up to 20 mg/hour. Three patients failed to respond even to higher doses and needed furosemide i.v. or furosemide + dobutamine. One patient died of cardiogenic shock. No changes in cardiac output, heart rate and blood pressure and no clinical side-effects were recorded. Thus, in acute cardiac failure ISDN may be effective in doses slightly superior to those of nitroglycerin, but increasing the dosage above 7 or 8 mg/hour does not bring additional benefits. The drug is remarkably well tolerated.

Acute Disease↗
PubMed1976

[Prophylactic effect of isosorbide dinitrate on postoperative cardiac complications (author's transl)].

Isosorbide dinitrate (ISD) was administered before, during and after 178 operations performed on 127 patients with arterial occlusive disease. Its influence on postoperative myocardial infarction, heart failure and mortality was tested by comparison with 188 operations performed on 140 patients with hypertension and/or old myocardial infarction receiving no ISD prophylaxis. Risk of cardiac complications was similar in both groups. Mortality in the ISD-treated group was significantly lowered as compared with the control group and was about half of the overall mortality in patients with arterial occlusive disease operated on at our hospital over the past 10 years. This difference depended partly on the influence of ISD on cardiac complications. Post-operative myocardial infarction during ISD prophylaxis occurred in 0.6% of cases as compared with 3.7% in the control group (p less than 0.05), whilst the respective values for postoperative heart failure were 5.7% and 18.2% (p less than 0.001). Both complications are related to absolute or relative hypoxia during the post-operative stress period. ISD is effective by lowering cardiac preload and afterload and thereby diminishing myocardial oxygen demand. ISD is the drug of choice for surgical patients since it provides a steady and long-lasting effect after sublingual absorption. ISD prophylaxis during the perioperative period is indicated in cases with coronary artery disease and with increased cardiac preload or afterload.

Arterial Occlusive Diseases↗
PubMed2001

Comparison between isosorbide dinitrate in aerosol and in tablets for the treatment of hypertensive emergencies.

Sixty patients with a hypertensive emergency (mean arterial pressure >130 mm Hg and evidence of target organ damage) were randomly divided into two groups of 30 patients each. Group A received 1.25 mg of isosorbide dinitrate aerosol upon arrival and a second dose 15 minutes later when the mean arterial pressure reduction was < 15%. Group B received a single 5 mg tablet of sublingual isosorbide dinitrate. Electrocardiography was performed in both groups prior to and 30 minutes after the medication. Blood pressure was monitored for 6 hours. Blood pressure in Group A patients decreased in an average time of 10 minutes from 191 +/- 12/122.3 +/- 5 to 151.5 +/- 9.2/93 +/- 4 mm Hg, p < 0.005. Mean arterial pressure decreased by 22.8%: 145 +/- 7 to 112 +/- 7.5 mm Hg, p < 0.005. No adverse effects occurred. Five patients in Group B did not respond; in the rest of the group blood pressure decreased 45 minutes after receiving the medication from 194 +/- 8/125 +/- 5.5 to 160 +/- 11/98 +/- 6 mm Hg; p < 0.005. Mean arterial pressure decreased by 20.1%: 148.3 +/- 12 to 118.6 +/- 9 mm Hg, p < 0.002; ten patients suffered headache. Three patients in Group A had a subepicardial lesion in the first electrocardiograph, which disappeared with the use of the aerosol. In Group B, electrocardiography results were normal. These results seem to indicate that isosorbide dinitrate aerosol is better than tablets for the treatment of patients with a hypertensive emergencies.

Administration, Inhalation↗
PubMed1997

[Influence of combination therapy (isosorbide dinitrate and molsidomine) on the incidence of angina pectoris in patients with coronary heart disease].

UNLABELLED: Angina pectoris in patients with severe 3-vessel-disease refractory to treatment is a challenge for the treating physician. We have therefore tested the treatment efficacy of isosorbide dinitrate combined with molidomine on the frequency of angina pectoris in patients with symptoms refractory to treatment. PATIENTS AND METHODS: 15 patients with severe coronary heart disease were included in the study. The protocol included a 2-weeks stabilisation phase, followed by a 4-weeks treatment phase with 100 mg isosorbide dinitrate in the morning as well as 8 mg slow-release molsidomine at 6 p.m. RESULTS: Initially all of the 15 patients reported about daily angina pectoris attacks. After 4 weeks of treatment 4 out of 15 patients became free of symptoms. From the other 11 patients 6 reported an improvement, 5 an unchanged frequency of attacks. DISCUSSION: Combination treatment with isosorbide dinitrate with molsidomine in a slow-release form (in the nitrate free interval) showed a distinct improvement in patients with angina pectoris refractory to treatment with reduction of complaints. The effect of the combination is possibly based on a prolonged vasodilatation of the stenosed vessels and a prolonged reduction of filling pressure (reduction of preload).

Aged↗
PubMed1989

Comparison of relaxation induced by glyceryl trinitrate, isosorbide dinitrate, and sodium nitroprusside in bovine airways.

Nitrates are generally regarded as bronchial smooth muscle relaxants. However, reports about the clinical efficacy of the nitrates in the treatment of asthma are conflicting. In the present study, the relaxant effects of glyceryl trinitrate, isosorbide dinitrate, sodium nitroprusside, and isoproterenol were measured and compared in vitro in airway preparations isolated from variously sized airways in bovine lung. Strips of trachealis from cervical and thoracic ends of the trachea and rings of intrapulmonary bronchi of various diameters (14 to 1 mm outer diameters) were mounted for recording of isometric tension. Submaximal tone was induced using 10(-6) M carbachol, and responses to cumulatively increasing concentrations of glyceryl trinitrate, isosorbide dinitrate, sodium nitroprusside, or isoproterenol were measured. Isoproterenol (10(-8) to 10(-4) M) was equiactive as a relaxant in all preparations. Glyceryl trinitrate (10(-7) to 10(-5) M) relaxed trachealis, but was progressively and significantly less effective as a relaxant as the diameters of the bronchial rings decreased. Although less potent than isoproterenol, sodium nitroprusside (10(-6) to 10(-4) M) was effective in relaxing all the airway preparations. Similar to glyceryl trinitrate, sodium nitroprusside was less effective in small than in large airways. However, the relationship between relaxant responses to sodium nitroprusside and airway size was not as marked as for glyceryl trinitrate. Isosorbide dinitrate at concentrations as great as 10(-5) M did not relax carbachol-induced tone in any of the bronchial rings and only induced a small amount of relaxation in trachealis at 10(-5) M.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗