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PubMed2001

Influence of endothelium in dose-dependent inhibition and potentiation by isoniazid of isosorbide dinitrate relaxation of rat aorta.

The influence of in vivo administration of isoniazid on the relaxant effect of isosorbide dinitrate was determined by pretreating rats with various doses of isoniazid and obtaining concentration-response curves to isosorbide dinitrate in aortic rings from these animals. In rings with endothelium, isoniazid potentiated responses to isosorbide dinitrate at doses of 10, 30, and 100 mg/kg; 3 and 300 mg/kg were without effect. In endothelium-denuded preparations, potentiation was present only at 10 mg/kg; 3 and 300 mg/kg inhibited relaxation. Other experiments indicated that isoniazid potentiation was prevented by pyridoxine, was reproduced with theophylline, and did not occur with 3-morpholinosydnonimine or papaverine. These results were deemed compatible with the hypothesis that isoniazid inhibits transsulfuration of homocysteine and causes its accumulation in vascular smooth muscle and endothelial cells, where it functions as a thiol intermediate and leads to enhanced bioactivation of isosorbide dinitrate. Potentiation appeared to occur only with moderate increases of homocysteine.

Animals↗
PubMedDate not supplied

Patient self-reporting of compliance does not correspond with electronic monitoring: an evaluation using isosorbide dinitrate as a model drug.

STUDY OBJECTIVE: To assess the accuracy of patient-kept diaries relative to electronic monitoring of compliance with isosorbide dinitrate prescribed 3 times/day for ischemic heart disease. DESIGN: Unblinded, prospective, three-phase study. METHODS: Patients with coronary artery disease prescribed isosorbide dinitrate 3 times/day were asked to record the time of administration of each dose in a pocket diary while being monitored for compliance with a computerized Medication-Event Monitoring System (MEMS-4) vial that electronically recorded the date and time the vial was opened. RESULTS: Sixty-eight stable outpatients with documented coronary artery disease who were prescribed isosorbide dinitrate 3 times/day were evaluated. Based on a prospectively chosen definition including a nitrate-free period, the mean (+/-SD) overall compliance rates were 71% (+/-30) versus 55% (+/-32) for the patient-kept diaries and the MEMS vials respectively (p = 0.001). The concordance between patient-kept diaries and MEMS data indicate that 67% of patients overestimate their compliance when using a self-recording tool. An average of 30% of diary entries were in error compared with the MEMS vial recordings. CONCLUSIONS: Patient-kept diaries statistically overestimate actual compliance relative to that determined by MEMS devices. Given the prevalence of the use of diaries as the predominant tool on which researchers depend to document compliance with study drugs, our findings suggest that this practice should be reevaluated specifically when the time of the dose and documentation of administration are critical to qualifying the outcome of drug therapy. Such is the case with isosorbide dinitrate use in patients with ischemic heart disease. Furthermore, the overall poor compliance documented in this study suggests that the utility of isosorbide dinitrate prescribed 3 times/day be reevaluated as a clinically effective antianginal drug.

Administration, Oral↗
PubMed2000

Changes in tumor oxygenation/perfusion induced by the no donor, isosorbide dinitrate, in comparison with carbogen: monitoring by EPR and MRI.

PURPOSE: In an effort to improve radiotherapy treatments, methods aimed at increasing the quantity of oxygen delivered to tumors were investigated. The aim of this study was to evaluate the effect of one nitric oxide (NO) donor (isosorbide dinitrate) on pO(2) and blood flow in a murine tumor model. The effect was compared to carbogen, used as a reference treatment. METHODS AND MATERIALS: Thirty-six liver tumors implanted in mouse thighs were imaged using magnetic resonance imaging (MRI) at 4.7 Tesla with dynamic Gd-DTPA and blood oxygen level-dependent (BOLD) contrast-enhanced imaging after administration of isosorbide dinitrate or carbogen. The effect on the pO(2) was also tested by EPR oximetry (1.1 GHz) on 52 mice. RESULTS: A significant increase in MRI intensity was observed for both treatments in comparison with the control group. EPR oximetry showed a dose-dependant increase in tumor pO(2) for isosorbide dinitrate (by 5.9 mmHg at 0.2 mg/kg) and a substantially greater change for carbogen breathing (by 23 mmHg). CONCLUSION: Both tumor blood flow and pO(2) were increased by isosorbide dinitrate and carbogen. Carbogen is more efficient than isosorbide dinitrate in increasing the BOLD image intensity, as well as the tumor pO(2), but as efficient as isosorbide dinitrate in the Gd-DTPA contrast-enhanced imaging. We conclude that the effects of carbogen on improving tumor pO(2) involve both improved blood flow and improved hemoglobin oxygenation, whereas the effects of isosorbide dinitrate are predominantly mediated by improved blood flow alone.

Animals↗
PubMed1990

Acute effects of nifedipine versus isosorbide dinitrate on exercise tolerance in patients with isolated coronary artery occlusion and collaterals.

The acute effects of slow-release nifedipine and isosorbide dinitrate on exercise tolerance were compared in nine patients with isolated total coronary artery occlusion showing retrograde filling via collaterals. All patients had a reproducible positive exercise stress test off medication before the study. Each patient was randomized to 10 mg slow-release nifedipine and 5 mg isosorbide dinitrate in a single-blind, cross-over study. The exercise stress test was performed 30 minutes after drug administration. After nifedipine, three patients had a negative exercise stress test, whereas the test was negative after isosorbide dinitrate only in one patient. A significantly higher exercise tolerance was detected at peak exercise after nifedipine than after isosorbide dinitrate, as shown by a longer exercise time (380 +/- 44 vs. 295 +/- 41 seconds, p less than 0.001), a more increased maximum work load (355 +/- 89 vs. 255 +/- 55 W x min, p less than 0.02), and a higher rate-pressure product (30,300 +/- 2,500 vs. 26,100 +/- 2,700, p less than 0.01). In conclusion, these results seem to suggest that nifedipine may have a vasomotor effect on collaterals, since it elevated the threshold of ischemia more than isosorbide dinitrate did in patients with isolated coronary artery occlusion, showing retrograde filling via collaterals.

Angina Pectoris↗
PubMed1983

A comparison of nifedipine and isosorbide dinitrate in angina pectoris with particular reference to arterial oxygen saturation.

To explore beneficial and harmful effects of various combinations of antianginal drugs, we compared antianginal and cardiorespiratory effects of nifedipine and isosorbide dinitrate in low and high doses in combination with nadolol, a long acting beta-adrenoceptor blocker in a double-blind study in 19 patients with stable angina pectoris. Nadolol alone and in combination with the other two drugs reduced anginal attack rate and glyceryl trinitrate consumption; the high dose isosorbide dinitrate showed a further significant (P less than 0.05) reduction in both but the high dose nifedipine did not show such a trend. sigma ST depression (all leads) was significantly (P less than 0.05) more reduced by the high dose nifedipine than by the same dose of isosorbide dinitrate in combination with nadolol. Nadolol reduced forced expiratory volume in one sec (FEV1) slightly and this effect was reversed both by isosorbide and nifedipine. Isosorbide dinitrate in combination with nadolol reduced the basal and post-exercise arterial oxygen saturation (SaO2) whereas nifedipine did not reduce the mean SaO2 below the pre-trial level. A significantly greater sigma ST depression was associated with a lower post-exercise SaO2 (less than or equal to 92%) during all treatment periods but the fall of SaO2 occurred more often during isosorbide than during nifedipine treatment periods. These studies show that both isosorbide dinitrate and nifedipine enhance antianginal efficacy of nadolol. Isosorbide dinitrate, unlike nifedipine, reduces SaO2 which is associated with a greater sigma ST depression.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Plasma concentrations of isosorbide dinitrate after cutaneous and sublingual doses to human subjects.

After application of 100 mg (nominal dose) isosorbide dinitrate as an ointment to the skin of human subjects, mean drug concentrations were 1 to 2 ng/ml for 1.5 hour and reached a peak of 6.2 ng/ml at 6 hours. Thereafter, mean concentrations declined slowly to 2.9 ng/ml at 12 hours and 1.2 ng/ml at 24 hours. After a sublingual dose of 5 mg isosorbide dinitrate, mean drug concentrations reached a peak of 15.9 ng/ml at 0.5 hour and declined with a half-life of about 50 minutes. The mean bioavailability of isosorbide dinitrate from the ointment was estimated as 30 per cent of that from the sublingual tablet when corrected for differences in dose/body weight ratio. The results demonstrate that concentrations of isosorbide dinitrate in plasma can be maintained for relatively long periods when the drug is applied to the skin.

Administration, Topical↗
PubMed2000

The effectiveness of tenoxicam vs isosorbide dinitrate plus tenoxicam in the treatment of acute renal colic.

OBJECTIVE: To determine the effectiveness of isosorbide dinitrate in combination with tenoxicam compared with tenoxicam alone for the relief of acute renal colic. PATIENTS AND METHODS: Fifty patients with acute renal colic were randomly and in a double blind fashion divided into two treatment groups of 25 each. Group 1 received tenoxicam (40 mg intravenously) and group 2 received tenoxicam (40 mg intravenously) plus sublingual isosorbide dinitrate (5 mg). The patients were compared for visual pain scores, heart rate and blood pressure between and within the groups before and after treatment. RESULTS: Comparing the groups, group 2 had significantly lower pain scores after treatment (P < 0.05) but no other variables were significantly different (P > 0.05 for each). Within the groups the pain scores were significantly lower after treatment in both groups (P < 0.05). Group 2 also had a significantly lower heart rate and blood pressure after treatment (P < 0.05). There were no side-effects caused by tenoxicam and isosorbide dinitrate in either group. CONCLUSION: The use of tenoxicam alone or combined with isosorbide dinitrate was effective in relieving of renal colic, but the relief obtained with the combination was significantly greater than tenoxicam alone.

Acute Disease↗
PubMed1997

Comparative efficacy of the intravenous administration of linsidomine, a direct nitric oxide donor, and isosorbide dinitrate in severe unstable angina. A French multicentre study. French Group of Investigators.

AIMS: Although linsidomine shares common properties with nitrovasodilators, it releases nitric oxide directly without catalytic involvement by thiols. We conducted a prospective, randomized, multicentre, parallel group, single-blind study to compare the efficacy of intravenous administration of linsidomine with that of isosorbide dinitrate in unstable angina. METHODS AND RESULTS: Between November 1990 and July 1992, 568 patients with suspected unstable angina (class IIIB of the Braunwald classification) received a continuous infusion of either linsidomine (1 mg.h-1 on average) or isosorbide dinitrate (2.5 mg.h-1 on average) for 72 h. All patients received concomitant aspirin and intravenous heparin, 81% beta-blockers and 38% calcium antagonists. Holter monitoring was performed in all patients and analysed blindly. Only 25% of the patients had at least one episode of chest pain during the study (24.6% vs 25.8% in the linsidomine and isosorbide dinitrate groups, P = 0.74), of which 12% were associated with ECG changes. Holter criteria yielded similar results in both groups: 33% of patients presented episodes of myocardial ischaemia (32.6% vs 33.9% in the linsidomine and isosorbide dinitrate groups, P = 0.74), while 45% showed episodes of ventricular arrhythmia (43.5% vs 46.5% in the linsidomine and isosorbide dinitrate groups, P = 0.48). The incidence of serious clinical events at 72 h (death, myocardial infarction or myocardial revascularization) was 6.5% (5% vs 8% in the linsidomine and isosorbide dinitrate groups, P = 0.17). CONCLUSION: Intravenous linsidomine is at least as efficacious as isosorbide dinitrate in the stabilization of patients with severe unstable angina.

Aged↗
PubMed1983

Treatment of portal hypertension with isosorbide dinitrate alone and in combination with vasopressin.

Experimental animal studies have suggested that certain vasodilators could minimize the adverse cardiovascular effects of vasopressin. We investigated the hemodynamic effects of isosorbide dinitrate, alone and in combination with vasopressin, in patients with liver cirrhosis. In 10 patients, isosorbide dinitrate, 5 mg sublingually, reduced portal pressure by 21% as assessed by the gradient between wedged and free hepatic venous pressure, but also decreased mean arterial pressure (MAP) by 20%, pulmonary artery wedge pressure (WP) by 50%, and oxygen delivery (DO2) by 13%. In 6 other patients, isosorbide dinitrate, 5 mg sublingually, combined with vasopressin, 0.4 U/min iv, reduced portal pressure by 37%, increased MAP by 13%, and mean pulmonary artery pressure (MPAP) by 70%, and decreased DO2 by 32%. Thus, isosorbide dinitrate reduces effectively portal hypertension in patients with liver cirrhosis, but also decreases DO2 to the tissues as a consequence of a fall in cardiac output due to decreased preload. At the dosage used in this study, isosorbide dinitrate does not prevent the adverse hemodynamic effects of vasopressin.

Adult↗
PubMed1988

Effects of intracoronary isosorbide dinitrate during acute myocardial ischaemia: a study during angioplasty.

The effects of isosorbide dinitrate on acute myocardial ischaemia were studied in 19 patients during coronary angioplasty. The duration of balloon inflation to the onset of ST segment depression was increased by the administration of intracoronary isosorbide dinitrate from (mean +/- SEM) 13 +/- 2 to 20 +/- 2 s (48%) (P less than 0.01) and the duration to 1 mm ST segment depression increased form 23 +/- 2 to 29 +/- 3 s (28%) (P less than 0.01). Systolic blood pressure fell from 118 +/- 3 to 111 +/- 4 mmHg but there was no change in intracoronary distal occlusion pressure. Thus during coronary occlusion isosorbide dinitrate prolongs the time to the onset of myocardial ischaemia.

Acute Disease↗
PubMed1997

Effects of amlodipine and isosorbide dinitrate on exercise-induced and ambulatory ischemia in patients with chronic stable angina pectoris.

This study was designed to compare once-daily administration of 5-10 mg amlodipine with two daily doses of 40 mg sustained-release isosorbide dinitrate in 59 patients with stable angina using a randomized, double-blind, crossover study design. Anginal episodes, nitroglycerin consumption, and possible adverse events were recorded in a diary. A maximal symptom-limited bicycle exercise test and 48-hour ambulatory ECG monitoring were performed at baseline and at the end of each 5-week period of therapy. Exercise time, time to angina, time to ST depression, and maximal ST depression were measured during exercise. During ambulatory monitoring, the number of ischemic episodes and the duration per hour of ST depression were assessed. Amlodipine significantly reduced anginal episodes (P < 0.001) when compared with isosorbide dinitrate. Furthermore, amlodipine prolonged time to ST depression (P < 0.001) and time to angina (P < 0.05) when compared with isosorbide dinitrate. The number and duration of ischemic episodes during ambulatory monitoring were significantly reduced with amlodipine when compared with baseline values (P < 0.05), whereas no differences were found between isosorbide dinitrate and baseline. Adverse events were reported more frequently with isosorbide dinitrate than with amlodipine (P < 0.02). Amlodipine appears to be more effective and tolerable than sustained-release isosorbide dinitrate as monotherapy for chronic stable angina.

Adult↗
PubMed1982

Oral isosorbide dinitrate in angina pectoris: comparison of duration of action an dose-response relation during acute and sustained therapy.

The effects of different oral doses of isosorbide dinitrate administered acutely and four times daily during sustained therapy were studied in 12 patients with angina pectoris. After administration of 30, 60 and 120 mg of isosorbide dinitrate, the average plasma concentrations were higher and the area under the plasma concentration time curve was greater during sustained than during acute therapy (p less than 0.01). Reduction in standing systolic blood pressure was greater during acute than during sustained therapy (p less than 0.001). This reduction in systolic blood pressure was dose-related and persisted for 8 hours during acute therapy, but was not dose-related and was demonstrable for only 4 hours during sustained therapy. Compared with placebo therapy, exercise duration to the onset of angina and to the development of moderate angina increased significantly after each dose of isosorbide dinitrate for 8 hours during acute therapy but for only 2 hours during sustained therapy. During acute therapy, administration of a single dose of 15 or 30 mg of isosorbide dinitrate produced similar improvement in exercise tolerance as did a dose of 60 or 120 mg. During sustained therapy (15 mg four times daily), exercise tolerance increased to the same magnitude as with doses of 30, 60 or 120 mg four times daily. In most patients, near maximal improvement in exercise tolerance occurred after a dose of 15 or 30 mg four times daily. It is concluded that during sustained therapy with isosorbide dinitrate, partial tolerance to the antianginal and circulatory effects develops rapidly.

Administration, Oral↗
PubMed1987

Coronary dilator effects of intracoronary nifedipine and isosorbide dinitrate.

Although both nitrates and calcium antagonists may be administered by the intracoronary route, the relative efficacy of these agents and of their combination is unknown. In this study, we investigated the coronary vasodilatory potential of intracoronary nifedipine, isosorbide dinitrate and their combination in patients undergoing routine coronary arteriography. Both normal and diseased segments of coronary arteries were studied. Coronary artery diameters were measured from 35 mm cine film before and after the administration of each drug. Two groups of 10 patients were studied: group I received nifedipine, 0.2 mg, followed by isosorbide dinitrate, 1 mg, group II received isosorbide dinitrate, 1 mg, followed by nifedipine, 0.2 mg. Both agents resulted in significant dilatation of normal and diseased segments of the coronary arteries when injected as the first drug, but neither nifedipine nor isosorbide dinitrate produced significant additional vasodilation when injected as the second drug. The degree of dilatation of both diseased and normal segments produced by either nifedipine or isosorbide dinitrate was similar, suggesting that the dose used, of either drug, produced near maximal coronary vasodilatation. Importantly, drug induced dilatation of stenotic segments was similar to that of normal segments.

Adult↗
PubMed1985

Comparative effects of captopril and isosorbide dinitrate on pulmonary arteriolar resistance and right ventricular function in patients with severe left ventricular failure: results of a randomized crossover study.

We compared the short-term hemodynamic effects of isosorbide dinitrate (40 mg orally) and captopril (25 mg orally) in 18 patients with severe chronic heart failure in a randomized, crossover study conducted on consecutive days. Captopril and isosorbide dinitrate produced similar decreases in systemic vascular resistance, but whereas nitrate therapy decreased pulmonary arteriolar resistance significantly, captopril did not; the difference between the two drugs was highly significant (-25% vs -5%, p less than 0.001). Left ventricular filling pressures declined similarly with both captopril (-10.5 mm Hg) and with isosorbide dinitrate (-9.3 mm Hg), but because pulmonary arteriolar resistance fell significantly with nitrate therapy, mean right atrial pressure decreased more with isosorbide dinitrate than with captopril (-5.4 vs -2.8 mm Hg, respectively; p less than 0.001). Although systemic resistance declined similarly with both drugs, cardiac index increased more with nitrate therapy than during converting-enzyme inhibition (+0.47 vs +0.23 L/min/m2) (p less than 0.01), and therefore mean arterial pressure fell less with isosorbide dinitrate than with captopril (-10.5 mm Hg vs -16.7 mm Hg); p less than 0.05); two patients developed symptomatic hypotension with captopril, whereas none did so with the nitrate. The difference in the effects of the two drugs on cardiac index was not due to differences in their effects on heart rate, since heart rate fell similarly with both drugs, and thus both drugs produced similar increases in stroke volume index. These data indicate that, in patients with severe chronic heart failure, nitrates exert favorable dilating effects on the pulmonary circulation not shared by captopril.(ABSTRACT TRUNCATED AT 250 WORDS)

Captopril↗
PubMed1985

Comparison of antianginal efficacy of nifedipine and isosorbide dinitrate in chronic stable angina: a long-term, randomized, double-blind, crossover study.

Using a double-blind, crossover design, the comparative efficacy and safety of nifedipine and isosorbide dinitrate in the treatment of stable angina were studied in 34 patients. The study included a 2-week placebo washout period and two 6-week periods during which patients were randomized to either nifedipine or isosorbide dinitrate. The doses were titrated for each patient, and mean doses of the 2 drugs were comparable. A time-limited thallium treadmill test was performed at the end of each phase. Ischemic zone count rates were normalized to those of the nonischemic zone, and the change in this ratio with redistribution was calculated as reversible thallium defect. Two patients were discontinued from the study within 1 week after initiation of isosorbide dinitrate because of severe, intolerable headache. Two patients were withdrawn while receiving nifedipine: one had new congestive heart failure and the other had increasing angina. Of the remaining 30 patients who tolerated both drugs for at least 1 week, 4 patients from the isosorbide dinitrate group were either prematurely crossed over or discontinued from the study because of headache. One patient suffered headache from both drugs and was discontinued from the study. In the 30 patients, only nifedipine significantly reduced resting arterial pressure compared with baseline. Further, only nifedipine therapy resulted in significant decreases in the rate-pressure product and systolic pressure at a given workload. However, significant decreases in angina frequency, nitroglycerin consumption and exercise-induced maximum ST-segment depression and reversible thallium perfusion defect were produced by both nifedipine and isosorbide dinitrate.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1981

Vasodilator treatment with isosorbide dinitrate and hydralazine in chronic heart failure.

Several reports have suggested that because isosorbide dinitrate and hydralazine have different and additive haemodynamic effects at rest in patients with chronic heart failure, these agents should be administered in combination. Some studies, however, indicate thay they are effective individually as well. Since most patients with heart failure are symptomatic only with activity, we examined the haemodynamic effects of these drugs given individually and in combination, at rest and during upright bicycle exercise. As has been noted previously, at rest isosorbide significantly lowered both ventricular filling pressures and did not change cardiac output; hydralazine increased cardiac output and had only a slight effect on pulmonary capillary wedge pressure; combined treatment produced both beneficial effects. In contrast, during exercise isosorbide dinitrate also raised cardiac output while hydralazine more dramatically lowered the wedge pressure. Combined treatment produced significantly greater improvement in each haemodynamic index than either drug alone, with a resulting 54 per cent increase in exercise cardiac output, and a 33 per cent reduction in exercise wedge pressure. Maximal oxygen consumption increased acutely during combined treatment. These findings suggest that isosorbide dinitrate and hydralazine may each be effective in some patients, but that they are even more beneficial in combination.

Adult↗
PubMed1981

Hydralazine and isosorbide dinitrate: comparative central and regional hemodynamic effects when administered alone or in combination.

Central and regional hemodynamic studies were performed before and after the oral administration of 75 mg of hydralazine and/or 20 mg of isosorbide dinitrate in 15 patients with low-output congestive heart failure. Hydralazine increased mean cardiac output 17-25%, mean renal blood flow 19%, and limb blood flow 17% (all p < 0.05). Mean hepatic blood flow did not change significantly with hydralazine. Except for a small increase in cardiac output (6%, p < 0.05) at 30 minutes, isosorbide dinitrate did not significantly alter central, renal, hepatic or limb blood flow. Combining isosorbide dinitrate and hydralazine effected similar increases in cardiac output (17-24%, p < 0.05), renal (17%, p < 0.05) and limb (20%, p < 0.05) blood flow as those elicited by hydralazine alone. The combination did not significantly alter mean hepatic blood flow. Hydralazine, alone or combined with isosorbide dinitrate, increases renal and limb blood flow in congestive heart failure in proportion to the augmented cardiac output; isosorbide dinitrate alone does not alter blood flow to these regions. Neither drug (or combination) changes hepatic blood flow in this clinical setting.

Adult↗
PubMed1985

Double-blind randomised crossover trial comparing isosorbide dinitrate cream and oral sustained-release tablets in patients with angina pectoris.

Percutaneous isosorbide dinitrate cream and sustained-release tablets were compared in a double-blind randomised crossover trial in 28 patients with coronary artery disease and chronic stable angina pectoris. Twenty-two patients completed the trial. Both preparations significantly increased the mean exercise time to the onset of angina (P less than 0.001) and to termination of exercise (P less than 0.001) compared to the pre-treatment period. There were no significant differences between the cream and tablets with respect to frequency of anginal attacks, glyceryl trinitrate consumption, heart rate and ST segment depression at the onset of angina, ST segment depression at maximal exercise and the double product of heart rate and systolic blood pressure at maximal exercise. Equal numbers of patients expressed preference for cream and tablets. We conclude that in this group of patients isosorbide dinitrate sustained-release tablets have no clinical advantage over isosorbide dinitrate cream which, may, therefore, be of particular value for those patients with angina pectoris who dislike taking tablets or who prefer this form of nitrate preparation.

Administration, Oral↗