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PubMed1993

[Effects of intravenous infusion of isosorbide dinitrate on hemodynamics during anesthesia and surgery].

Ninety nine patients with ischemic changes of the heart on preoperative and intraoperative ECG tracings were studied to evaluate effects of intravenous infusion of isosorbide dinitrate on hemodynamics during anesthesia and surgery. These patients ranging in ages from 24 to 80 years were administered intravenous isosorbide dinitrate at a rate of either 0.5 or 1 microgram.kg-1 x min-1 during anesthesia and surgery. Arterial blood pressure was not influenced with intravenous isosorbide dinitrate at the speed of 0.5 microgram.kg-1 x min-1 during anesthesia and surgery. The arterial pressure of the patients decreased slightly but significantly 30 min after the start of 1 microgram.kg-1 x min-1 of isosorbide dinitrate infusion, but it recovered to the control level at the end of administration of isosorbide dinitrate. Heart rate was unchanged with intravenous isosorbide dinitrate during anesthesia and surgery in both groups, except a mild increase at the end of isosorbide dinitrate infusion of 1 microgram.kg-1 x min-1. Arterial blood oxygen tension showed no decrease during the administration of isosorbide dinitrate and no adverse reactions associated with administration of the drug was detected in this study. Significant improvement of ischemic changes on ECG tracings were observed in about 25% of the patients who received 1 micrograms.kg-1 x min-1 of intravenous isosorbide dinitrate.

Adult↗
PubMed1995

Effect of isosorbide dinitrate on gastroesophageal reflux in healthy volunteers and patients with Chagas' disease.

The effect of isosorbide dinitrate (ISD) on gastroesophageal reflux and gastric emptying during the 24-min period following a liquid meal was studied in healthy volunteers, Chagas' disease patients with normal esophageal motility (CD-1 group), and Chagas' disease patients with esophageal dysmotility (CD-2 group) with dynamic scintigraphy. At random, on two separate days, the subjects received 5 mg isosorbide dinitrate or an identical-appearing placebo tablet, by the sublingual route, and ingested a liquid test meal containing [99mTc]phytate colloid before scintigraphic studies were performed. Gastroesophageal reflux episodes were more frequent (P = 0.016) and gastroesophageal reflux indexes were greater (P < 0.010) after isosorbide dinitrate than after placebo in CD-2 group (N = 15) but not in healthy volunteers (N = 14) or CD-1 group (N = 9); six of seven CD-2 patients presenting with gastroesophageal reflux after isosorbide dinitrate had abnormal clearance of refluxate. Gastric emptying was similar in healthy volunteers (N = 13), CD-1 patients (N = 6), and CD-2 patients (N = 13), and no effect of isosorbide dinitrate on it was detected in any of the groups. In separate studies, 5 mg isosorbide dinitrate reduced the lower esophageal pressure (P < 0.01) in seven CD-2 patients. These results indicate that ISD increases the tendency towards GER in CD-2 patients, but not in healthy volunteers or CD-1 patients. This effect is probably related to an exceedingly intense relaxation of the LES caused by ISD in CD-2 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1979

Sustained effect of orally administered isosorbide dinitrate on exercise performance of patients with angina pectoris.

The efficacy of oral isosorbide dinitrate was evaluated in nine hospitalized patients with chronic angina pectoris and positive maximal bicycle exercise tests. Patients were randomized double-blind to receive either 20 mg of isosorbide dinitrate or placebo on successive days after a control maximal upright bicycle exercise test. On each day hourly exercise tests were performed for 4 hours after drug administration to an end point of fatigue or angina pectoris. Mean systolic blood pressure 4 hours after the administration of isosorbide dinitrate was 25 mm Hg less than the control value (P less than 0.001). The values for resting heart rate and exercise-attained heart rate-blood pressure product were not significantly different from the values after placebo. The duration of exercise was prolonged (P less than 0.025) for at least 3 hours, and less ST depression (P less than 0.01) was observed up to 3 hours after the administration of isosorbide dinitrate compared with control values. The demonstration of sustained imporved exercise performance and previously described hemodynamic effects with the use of higher doses suggests that adequate blood levels of isosorbide dinitrate or mononitrate metabolites may be important for the efficacy of oral organic nitrates.

Administration, Oral↗
PubMed1995

Solid-phase extraction of isosorbide dinitrate and two of its metabolites from plasma for gas chromatographic analysis.

A rapid, accurate and selective method for the determination of isosorbide dinitrate and its 2- and 5-isosorbide mononitrate metabolites in 1.0 ml of human plasma has been developed. Before chromatographic quantitation by gas-liquid chromatography with electron-capture detection, the compounds are subjected to solid-phase extraction, using ENVI 18 cartridges (Supelco). The intra-day and inter-day coefficients of variation are less than 10%, except the inter-day coefficient of variation for the assay of 5-isosorbide dinitrate which is less than 15%. Limits of quantitation are 10, 10 and 20 ng/ml for isosorbide dinitrate, 2-isosorbide mononitrate and 5-isosorbide mononitrate, respectively. Recoveries are in excess of 90% for isosorbide dinitrate and 70% for its two metabolites.

Chromatography, Gas↗
PubMed1991

Oral administration of isosorbide dinitrate inhibits arterial thrombosis in rats.

The effect of isosorbide dinitrate, a nitrovasodilator known to inhibit platelet function, was examined in a model of electrically induced carotid artery thrombosis in rats. In the dose range of 1-30 mg/kg isosorbide dinitrate, administered orally, significantly delayed carotid occlusion. These results demonstrate that isosorbide dinitrate has antithrombotic activity and it is suggested that this antithrombotic activity is due to the generation of nitric oxide.

Administration, Oral↗
PubMed1996

Role of pentobarbitone anaesthesia and sympathetic tone in the haemodynamic effects of isosorbide dinitrate in rats with cirrhosis.

The haemodynamic effects of nitrovasodilators and their mechanisms of action on portal hypertension remain unclear. The splanchnic and systemic haemodynamic response to the infusion of isosorbide dinitrate (100 micrograms/kg per min), a nitrovasodilator, was investigated in cirrhotic rats. The role of the conscious state in the haemodynamic response to isosorbide dinitrate was examined using rats that were anaesthetized with pentobarbitone. The role of sympathetic tone in the haemodynamic response to isosorbide dinitrate was examined using rats pretreated with the ganglion blocker hexamethonium. Isosorbide dinitrate had no haemodynamic effects in conscious, unblocked normal and cirrhotic rats. Isosorbide dinitrate had no haemodynamic effects in normal and cirrhotic rats treated with hexamethonium. In normal anaesthetized rats, isosorbide dinitrate significantly decreased systemic vascular resistance (414 +/- 25 vs 290 +/- 26 dyn.s/cm-5 per 100 g). In cirrhotic anaesthetized rats, isosorbide dinitrate significantly decreased mean arterial pressure (98 +/- 6 vs 79 +/- 7 mmHg), systemic vascular resistance (318 +/- 30 vs 207 +/- 10 dyn.s/cm-5 per 100 g), portal pressure (14.0 +/- 1.0 vs 11.3 +/- 0.9 mmHg) and portal territory vascular resistance (1362 +/- 163 vs 1031 +/- 182 dyn.s/cm5 per 100 g). In conclusion, this study shows that the portal hypotensive effects of isosorbide dinitrate depend upon the alterations of vascular tone by pentobarbitone.

Adjuvants, Anesthesia↗
PubMed1992

[Pharmacokinetics and pharmacodynamics of a new 80 mg oral delayed-action isosorbide dinitrate preparation].

A new galenic form of isosorbide dinitrate (consisting of a hydrophilic matrix which allows very slow release of the active drug) was studied from the pharmacokinetic and pharmacodynamic view points in 11 patients with stable angina pectoris under betablocker therapy. After testing their sensitivity to nitrates with a sublingual trinitrin test causing a fall greater than or equal to 20 mmHg in systolic and greater than or equal to 10 mmHg in diastolic blood pressure, the patients were given a single tablet of Risordan LP 80 daily for 7 days. The equilibrium plasma concentrations of isosorbide dinitrate and its mononitrate metabolites (2-isosorbide mononitrate and 5-isosorbide mononitrate) over 24 hours were measured on the 6th treatment day. A method of measuring these nitrate derivatives has been developed and validated. The concentrations measured enabled the study of the pharmacokinetics of this new form, showing an average minimal concentration of 5-isosorbide mononitrate (principal metabolite) of 85 +/- 41 micrograms/l and an amplitude of fluctuation over the 24 hours period of 296 +/- 102 micrograms/l. From the pharmacodynamic point of view, the evaluation of the sensitivity to a single dose of 0.75 mg of trinitrin 24 hours after the first dose of Risordan LP 80, just before the second dose and 24 hours after the seventh dose, showed a significant difference (average decrease of 40 +/- 19 mmHg in systolic blood pressure) with respect to the values observed during the selection phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1975

Isosorbide dinitrate. Effect on the vasodilator response to nitroglycerin.

To evaluate whether there is cross-tolerance to the circulatory effects of isosorbide dinitrate and nitroglycerin, six subjects were given 120 mg/day of sustained-action isosorbide dinitrate in three divided doses for six to eight weeks. Prior to and during the last week of long-term isosorbide dinitrate administration, the effects of sublingually given nitroglycerin (0.9 mg) on plethysmographically measured calf blood flow and venous volume at 30 mm Hg (VV[30]) were measured on three occasions and averaged. Although the arteriolar dilation produced by nitroglycerin was unaltered by isosorbide dinitrate, the venodilation was significantly attenuated. The VV[30] increased from 3.00 to 3.28 ml/100 ml (P less than .02) with nitroglycerin prior to isosorbide dinitrate administration, but failed to increase with nitroglycerin during the long-term administration of isosorbide dinitrate (2.95 to 2.95 ml/100 ml, P greater than .5).

Administration, Oral↗
PubMedDate not supplied

Isosorbide dinitrate in experimental portal hypertension: a study of factors that modulate the hemodynamic response.

Isosorbide dinitrate, a long-acting vasodilator, has been tested in human portal hypertension with conflicting results. In order to determine some of the factors that could affect the individual response to this drug, we infused isosorbide dinitrate at a low dose (10 to 25 micrograms per kg per min) and a high dose (100 micrograms per kg per min) to rats with portal vein stenosis. Under pentobarbital anesthesia, portal pressure was measured with an ileocolic vein catheter while cardiac output and regional blood flows were measured with the microsphere technique. At a dose that decreased arterial pressure by approximately 10%, cardiac output remained unchanged while portal vein inflow decreased significantly; portal pressure was not reduced (10.7 +/- 0.2 vs. 10.0 +/- 0.3 mm Hg), indicating a rise in portal vascular resistance. At a high dose of isosorbide dinitrate, arterial pressure and cardiac output fell markedly; portal pressure decreased only modestly (11.3 +/- 0.3 vs. 9.8 +/- 0.6 mm Hg, p less than 0.05), but portal flow was unchanged, indicating a reduction in portal vascular resistance. In addition, portal hypertensive rats received a constant i.v. infusion of N-acetyl-cysteine; the combination of the latter and isosorbide dinitrate markedly potentiated the effects on arterial pressure. Thus, the dose of the drug and the presence of cysteine-containing compounds appear to modulate the hemodynamic response to isosorbide dinitrate. Clinical testing with this drug should be undertaken with consideration of these factors.

Acetylcysteine↗
PubMed1994

Intravenous isosorbide dinitrate inhibits neutrophil aggregation and plasma-mediated stimulation of superoxide anion production.

Polymorphonuclear neutrophils are known to be activated during myocardial ischaemia causing release of free oxygen radicals and capillary plugging by cell aggregates and therefore to exacerbate ischaemic myocardial injury. Nitric oxide has been shown to modulate neutrophil activation within the ischaemic myocardium and therefore reduce myocardial injury during ischaemia. Drugs that act as nitric oxide donors may therefore modify neutrophil activation. We evaluated the effect of intravenous treatment with isosorbide dinitrate on neutrophil aggregation and plasma-mediated stimulation of neutrophil superoxide anion production in patients with ischaemic heart disease. Samples were obtained from patients before treatment and 15 and 30 min after receiving intravenous isosorbide dinitrate. Isosorbide dinitrate decreased neutrophil aggregation visualized in whole blood (25.3 +/- 3.6, 19.0 +/- 2.6 and 18.5 +/- 2.6 per 300 cells, respectively, P < 0.01). When patient's plasma was incubated with neutrophils obtained from healthy donors, superoxide anion release was 18.99 +/- 6.23, 11.38 +/- 2.79 and 11.49 +/- 3.15 nmol O2-/10(6) cells, respectively (P < 0.01). Therefore, intravenous isosorbide dinitrate inhibited both plasma-mediated stimulation of neutrophil superoxide anion production and neutrophil aggregation.

Adult↗
PubMed1994

The interaction of alpha-human atrial natriuretic peptide (ANP) with salbutamol, sodium nitroprusside and isosorbide dinitrate in human bronchial smooth muscle.

1. Contractions in human bronchial rings evoked by methacholine (10(-6) M) were reversed by single contractions of alpha-human atrial natriuretic peptide (10(-6) M), salbutamol (10(-6) M), sodium nitroprusside (10(-6) M) or isosorbide dinitrate (4.2 x 10(-5) M) and the extent of the relaxations compared. The activity of combinations of ANP with salbutamol, sodium nitroprusside and isosorbide dinitrate were compared with those for each agonist alone. 2. ANP and salbutamol were equipotent in reversing methacholine-evoked contraction and, in combination these agonists evoked an additive response. ANP and sodium nitroprusside also evoked similar degrees of relaxation and were additive, as were ANP and isosorbide dinitrate; however, with isosorbide dinitrate a higher concentration was required to evoke the same degree of relaxation as ANP, sodium nitroprusside or salbutamol. 3. Cumulative concentration-response curves to methacholine (10(-9)-3 x 10(-4) M) were examined in the presence and absence of the above bronchodilator substances, alone and in combination allowing their abilities to protect against contraction to be compared. ANP (10(-6) M) and salbutamol (10(-6) M) each attenuated subsequent contractions evoked by methacholine, an ability not shared with sodium nitroprusside (10(-6) M) or isosorbide dinitrate (4.2 x 10(-5) M). Indeed at lower concentrations of methacholine (< 3 x 10(-7) M), sodium nitroprusside evoked a paradoxical enhancement of methacholine-evoked contractions. 4. In combination, ANP and salbutamol attenuated contractions evoked by methacholine to a significantly greater degree than that seen with either agonist alone, whilst a combination of ANP and sodium nitroprusside evoked no greater effect than that seen with ANP alone. By contrast, isosorbide dinitrate and ANP together evoked a greater inhibition than ANP alone.5 These results suggest that a combination of agents such as ANP and salbutamol evokes a greater effect than either alone, both in reversing and protecting against methacholine-evoked contractions.Such combinations may be of benefit in the treatment of patients, allowing lower doses of drug to be used. Combinations of ANP and isosorbide dinitrate may likewise be of interest; however, the mechanism underlying the enhancement of ANP responses by isosorbide dinitrate requires further study.

Albuterol↗
PubMed1994

The antianginal efficacy of isosorbide dinitrate therapy is maintained during diuretic treatment.

OBJECTIVES: To determine whether the use of a diuretic would maintain the antianginal efficacy of isosorbide dinitrate during 1 week of therapy. METHODS: During continuous therapy, organic nitrates have a reduction in antianginal effectiveness and cause fluid retention. The study was a randomized, double-blind, placebo-controlled crossover design examining the effect of 1 week of daily treatment with 50 mg hydrochlorothiazide/5 mg amiloride on the antianginal effectiveness of 30 mg isosorbide dinitrate administered every 6 hours. Exercise stress testing was performed before and 3 hours after administration of isosorbide dinitrate at the start and end of the placebo and diuretic treatment phases. RESULTS: The time to onset of angina (475 +/- 35 versus 490 +/- 29 seconds, difference not significant) and to moderate angina after administration of isosorbide dinitrate (542 +/- 40 versus 566 +/- 37 seconds, difference not significant) were similar at the start and end of the diuretic phase of the study but were reduced at the end of the placebo phase (471 +/- 40 versus 410 +/- 40 seconds, p < 0.05 and 531 +/- 38 versus 466 +/- 39 seconds, p < 0.05, respectively). Total exercise time and time to onset of angina 3 hours after administration of isosorbide dinitrate were longer (p < 0.005) at the end of the diuretic phase compared with the end of the placebo phase. Patients gained weight during the placebo phase and lost weight during the diuretic phase of the study. The change in weight was inversely correlated to the change in total exercise time (r = -0.53, p < 0.05). CONCLUSIONS: Patients using a diuretic with isosorbide dinitrate maintain an increased anginal threshold and total exercise time compared with placebo. Weight change is inversely related to exercise duration, and this result is consistent with fluid retention restoring cardiac preload during nitrate use. The increased anginal threshold during concurrent isosorbide dinitrate and diuretic use may be attributable to maintenance of the organic nitrate-induced reductions in cardiac preload.

Aged↗
PubMed1997

Influence of the vasodilator drug isosorbide dinitrate on ocular circulation.

OBJECTIVE: To evaluate the ocular hemodynamic effects of the vasodilator drug isosorbide dinitrate. DESIGN: Randomized, prospective, controlled clinical trial assessing the short-term effects of 1 tablet containing 40 mg of isosorbide dinitrate vs placebo. SETTING: Department of Ophthalmology, University of Giessen, Germany. MAIN OUTCOME MEASURES: Systolic ophthalmic artery pressure (SOAP), systolic ocular perfusion pressure (SOPP), ocular pulsation amplitude (OPA), product of OPA x heart rate (HR), intraocular pressure (IOP), systolic and diastolic brachial artery pressure (SBAP and DBAP). Measurements were performed before and up to 7 hours after patients received the medication. PARTICIPANTS: Twenty healthy subjects (mean age, 28 years) who provided informed consent. RESULTS: After isosorbide dinitrate administration, SBAP, SOAP, and SOPP were significantly lowered (P = .01), and IOP tended to be lower (P = .08) compared with placebo. Maximum reduction was 3 to 5 hours after medication: SBAP was reduced by 10.9 mm Hg (9% reduction; P = .01), SOAP was reduced by 12.5 mm Hg (14% reduction; P = .01), SOPP was reduced by 11.3 mm Hg (14.5% reduction; P = .01), and IOP by 1.5 mm Hg (12% reduction; P = .08). The relation between SBAP and SOAP was significantly linear (P < .001), the correlation coefficient was 0.39. The DBAP remained unchanged, and the HR increased by 4 to 7/min (P = .08). The OPA and the product OPA x HR were significantly decreased (P < .001; P = .002) by maximum values of 44% and 40%, respectively. CONCLUSIONS: Administration of isosorbide dinitrate reduced SOAP and SOPP, reflecting reduced systemic systolic blood pressure. The decrease in OPA and the product OPA x HR (a measure of pulsatile ocular blood flow) may reflect a reduction in cardiac stroke volume typical for nitrates. Due to these hemodynamic effects and the minute reduction in IOP, the vasodilator drug isosorbide dinitrate, which has been proposed for glaucoma therapy, may be used only with caution in patients with glaucoma.

Adult↗
PubMed1976

Comparative effects of nitroglycerin and isosorbide dinitrate on coronary collateral vessels and ischemic myocardium in dogs.

To determine the effect of isosorbide dinitrate or ischemic myocardium, this agent was administered to dogs with well developed coronary collateral vessels 8 to 14 weeks after embolization and subsequent occlusion of the left anterior descending coronary artery. After thoracotomy the left coronary artery was cannulated and perfused with blood from the femoral artery. The distal left anterior descending artery was cannulated to monitor peripheral coronary pressure. Regional contractile force in the normal left circumflex and potentially ischemic left anterior descending regions was measured with isometric strain gauge arches sewn to the epicardium. Moderate decreases in coronary perfusion pressure averaging 27 mm Hg produced selective ischemia in the myocardium beyond the site of occlusion of the left anterior descending artery. Under these conditions the average increase in peripheral coronary pressure produced by intracoronary injection of isosorbide dinitrate was 9.0 mm Hg, whereas contractile force in the ischemic region increased by 30 percent. The contractile force was unchanged in the normal regions. Therefore, isosorbide dinitrate can dilate coronary collateral vessels and improve contractile force in ischemic areas. Intracoronary injection of nitroglycerin had similar effects. The durations of responses to isosorbide dinitrate and nitroglycerin were remarkably similar: 6.4 and 6.7 minutes, respectively. Although isosorbide dinitrate can directly dilate coronary collateral vessels, its effects are not longer lasting than those of nitroglycerin.

Animals↗
PubMed1994

Hemodynamic effects of combined treatment with somatostatin analogue (SMS 201-995) and low-dose isosorbide dinitrate on portal hypertension in conscious cirrhotic rats.

The authors investigated whether combined treatment with the somatostatin analogue, SMS 201-995, and low-dose isosorbide dinitrate enhanced the hemodynamic effects of the individual agents on rats with thioacetamide-induced cirrhosis. Four groups of cirrhotic rats received SMS 201-995 (0.1 microgram.min-1.kg-1), isosorbide dinitrate (10 micrograms.min-1.kg-1), both agents, or placebo, respectively. Hemodynamics were measured serially in conscious rats, using a radioactive microsphere method. SMS 201-995 reduced portal venous inflow 21 +/- 4% and portal pressure 17 +/- 3%. Isosorbide dinitrate decreased portal venous inflow 20 +/- 4%, by inducing splanchnic vasoconstriction mediated by low pressure baroreflexes, and this agent also decreased portal pressure, by 14 +/- 2%. Portal venous resistance rose 7.6 +/- 3% with isosorbide dinitrate alone, but decreased 18 +/- 4% with combination therapy. This effect may have been induced by the pronounced vasodilatory effect of isosorbide dinitrate on the venous vasculature, since the reflex splanchnic vasoconstriction that occurs with low-dose isosorbide dinitrate disappears when this agent is combined with SMS 201-995. The decrease in portal pressure was more marked (22 +/- 4%) and changes in systemic hemodynamics were milder with the combined treatment. It was concluded that combination therapy with SMS 201-995 and low-dose isosorbide dinitrate may be beneficial for portal hypertension in liver cirrhosis.

Analysis of Variance↗
PubMed2002

A comparison between the effects of diltiazem and isosorbide dinitrate on digoxin pharmacodynamics and kinetics in the treatment of patients with chronic ischemic heart failure.

OBJECTIVE: To evaluate the effect of an arteriolar dilator (diltiazem hydrochloride) versus a venodilator (isosorbide dinitrate) on digoxin kinetics and to estimate the efficacy and tolerability of these vasodilators when combined with digoxin for 10 days therapy in patients with congestive heart failure secondary to ischemic heart disease. METHODS: A double blind randomized cross over study was carried out to investigate the effect of an arteriolar dilator (diltiazem hydrochloride 180 mg/day orally) versus a venodilator (isosorbide dinitrate 30 mg/day orally) on digoxin kinetics (0.25 mg/day orally), after 10 days therapy in patients with heart failure due to ischemic heart disease. Also, the effect of these drugs on blood pressure, heart rate, renal functions and serum electrolytes, and their efficacy and tolerability in combination with digoxin were studied. This study was carried out in the Department of Medicine, Main Alexandria University Hospital, Alexandria, Egypt, during the period May 1999 through to May 2000. RESULTS: Diltiazem caused a significant increase in digoxin maximum serum concentration without significant change in time to reach maximum concentration and the apparent volume of distribution. The total digoxin clearance was significantly reduced and the elimination half life was prolonged. Subsequently the area under time-concentration curve and the steady-state digoxin level were increased, but were still within therapeutic margin. On the other hand isosorbide dinitrate significantly increased digoxin maximum serum concentration but without change in the other digoxin pharmacokinetic parameters. Isosorbide dinitrate, but not diltiazem, caused significant reduction in supine and standing blood pressure, while both drugs did not significantly alter pulse rate, renal functions, serum sodium potassium and electrocardiographic pattern. CONCLUSION: Patients who received diltiazem displayed a mean 51% increase in the area under the plasma concentration-time curve, 50% increase in mean steady state serum digoxin concentration, and 37% increase in peak serum digoxin concentration. While patients who received isosorbide dinitrate showed only a 15% increase in digoxin maximum serum concentration and no statistically significant change in mean steady state digoxin concentration or area under the plasma concentration-time curve. The elimination half life during the diltiazem phase was prolonged by 29% while there was no significant change with isosorbide dinitrate. Netiher diltiazem or isosorbide dinitrate significantly altered the time to reach maximum serum digoxin concentration. The addition of a vasodilator such as, diltiazem or isosorbid dinitrate to digoxin could significantly improve the symptoms and signs of heart failure compared to digoxin alone. They were well tolerated and without fear of electrolyte imbalance which potentiate digoxin toxicity.

Analysis of Variance↗
PubMedDate not supplied

Plasma concentrations and bioavailability of isosorbide dinitrate and pindolol from a combination formulation.

The plasma concentrations and bioavailability of sustained-release isosorbide dinitrate and standard-release pindolol have been compared after administration of these drugs in combination and alone. Bioavailability parameters of isosorbide dinitrate and pindolol obtained after administration of the drugs in combination were not significantly different (P greater than 0.05) to those obtained after administration of either drug alone. Two peaks of mean concentrations of isosorbide dinitrate occurred in plasma after administration of 30 mg of this drug in combination with 7.5 mg pindolol (4.4 ng ml-1 at 1 h and 4.5 ng ml-1 at 5 h), or alone (5.9 ng ml-1 at 2 h and 5.7 ng ml-1 at 5 h). In each case, plasma concentrations of isosorbide dinitrate were maintained during at least 8 h, whereas the drug was not detected in plasma at 2.5 h after administration of a standard-release formulation. The peaks of mean concentrations of pindolol were 39.7 ng ml-1 at 1.5 h after administration of 7.5 mg drug in combination with isosorbide dinitrate and 38.0 ng ml-1 at 1 h administration of the drug alone. Concentrations of pindolol in plasma declined with a half-life of 3 h.

Adolescent↗
PubMed1988

Effects of isosorbide dinitrate on thromboxane A2 synthesis in carbon dioxide exposed platelets.

Isosorbide dinitrate (Nitorol R, 100 nmol/l) blocked an increase in thromboxane B2 concentration in human platelet-rich plasma caused by exposure to high CO2 tension, in the presence of arachidonic acid. Thromboxane B2 concentrations obtained at 1 or 2 mmol/l or arachidonic acid were not influenced by isosorbide dinitrate at low CO2 tension. Inhibitory action of isosorbide dinitrate on the thromboxane A2 synthesis appears to have a close relation to the site of CO2 action.

Blood Platelets↗