Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Isosorbide”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,207 records · Page 67Linked to original sources

The effect of intermittent administration of sustained release isosorbide dinitrate (sr-ISDN) in rats with volume overload heart.

Recently, it has been reported that intermittent administration of nitrate, with a nitrate-free interval of 10 to 12 hr eliminated expression of tolerance, and maintained its hypotensive effect. In the present study, we evaluated whether nitrate tolerance developed or not with an intermittent administration of sr-ISDN (5 mg/kg/ once a day) in Wistar rats. The effect of this administration protocol for sr-ISDN on the volume overload heart model, aortovenous fistula, was also examined. Furthermore, blood pressure was monitored by radio telemetry during sr-ISDN (5 mg/kg/once a day) administration. Nitrate tolerance did not develop, and eccentric hypertrophy due to volume overload was moderated by sr-ISDN administration. Sr-ISDN administration maintained blood pressure lower level than the placebo group. In conclusion, prolonged intermittent administration of sr-ISDN maintained its hypotensive effect during the entire experiment period, without developing tolerance, and moderated efferent hypertrophy with attenuated volume overload.

Analysis of Variance↗

The effects of antianginal drugs on left ventricular function in patients with effort angina pectoris. Comparison among isosorbide dinitrate, nifedipine and propranolol by PANOVA.

To study the acute effects of ISDN, nifedipine, propranolol and placebo on cardiac function in patients with myocardial ischemia and to characterize their hemodynamic effects by PANOVA, we repetitively performed exercise radionuclide angiography (RNA) following random assignment of each drug in 20 patients with effort angina pectoris. We obtained exercise response curves of hemodynamic parameters determined by RNA. ANOVA was performed to analyze the sizes (average height) of those response curves, and PANOVA (principal component analysis, PCA, combined with ANOVA) to analyze differences in the profiles (patterns) of the curves. By conventional analysis of variance followed by a Scheffé type multiple comparison, end-diastolic volume after ISDN, which was significantly smaller than those after the other drugs at rest (p less than 0.01), was similar to those after nifedipine and propranolol during exercise (96.4 +/- 4.6 ml/m2 vs. 94.8 +/- 5.1 ml/m2 and 97.1 +/- 4.9 ml/m2, respectively). Systemic vascular resistance after nifedipine, which was also significantly lower than those after the other drugs at rest (p less than 0.05), was not different from that after placebo during exercise (16.9 +/- 1.1 units vs. 18.7 +/- 1.3 units). Thus, this analysis was considered insufficient to fully differentiate the characteristics of each drug. By PANOVA, the profiles of LVEF with these three antianginal drugs were similar, and significantly differentiated from that of placebo (p less than 0.05). This indicated that the antianginal effect could be represented by the profiles of the response curves of LVEF, using PANOVA. Evaluating the underlying hemodynamic mechanisms of these drugs by PANOVA, ISDN was significantly differentiated from nifedipine and propranolol by the profile of end-diastolic volume (p less than 0.05). The characteristics of nifedipine were clearly demonstrated by the size and profile of systemic vascular resistance, and those of propranolol were also differentiated by the size and profile of the double product and P-V index. Hence, it is concluded that with the aid of PANOVA, the changes in hemodynamic parameters during ischemia can be evaluated in a manner that is highly effective in differentiating the characteristics of the effects of antianginal drugs in patients with angina pectoris.

Aged↗

Effect of isosorbide dinitrate infusion on the canine left ventricular force-length relationship.

Recently, the slope (Ec) of the left ventricular (LV) end-systolic force-diameter (Fes-Des) relationship has been proposed as a new index for assessing myocardial contractility. Using this relationship, the effects of ISDN on LV myocardial contractility were evaluated in 10 healthy adult mongrel dogs. After the intravenous infusion of propranolol and atropine to produce autonomic blockade, the inferior vena cava was gradually occluded for 20 sec to decrease preload while the dogs were kept apneic. The LV diameter was measured by ultrasonic crystals and LV pressure was measured by a micromanometer. After the control measurements, the dogs received intravenous ISDN (1, 5, 10, or 50 micrograms/kg/min), and inferior vena caval occlusion was repeated. Ec and the extrapolated diameter intercept (D0) of the LV Fes-Des relationship were determined for each dog from the end-systolic data. The differences in heart rate between the control state and ISDN infusion at any dose were not statistically significant. The Ec and D0 values also showed no significant changes with ISDN infusion (Ec: 80 +/- 19, 83 +/- 20, 84 +/- 17, 82 +/- 24, and 87 +/- 24 g/cm for 0, 1, 5, 10, and 50 micrograms/kg/min, respectively. D0: 1.38 +/- 0.42, 1.38 +/- 0.40, 1.38 +/- 0.38, 1.34 +/- 0.40, and 1.36 +/- 0.40 cm for 0, 1, 5, 10, and 50 micrograms/kg/min, respectively). These findings suggested that intravenous ISDN did not affect myocardial contractility in the normal in situ canine left ventricle.

Animals↗

Glyceryl trinitrate (nitroglycerin) ointment and isosorbide dinitrate: a review of their pharmacological properties and therapeutic use.

Sublingual glyceryl trinitrate (nitroglycerin) is the most widely used drug in the treatment of angina pectoris, but its use is limited due to its short acting effect. Recent investigations have shown that some longer acting nitrates administered orally or topically have a long acting antianginal effect. The mechanism of the antianginal effect of nitrates is multifactorial. Nitrates increase oxygen supply to the myocardium by causing redistribution of coronary blood flow. In addition, nitrates decrease myocardial oxygen demand by reducing left ventricular volume, intramyocardial tension, and left ventricular afterload. The use of nitrates for the treatment of congestive heart failure has also been established in recent years. Nitrates have a predominant venodilatory effect resulting in peripheral blood pooling and decreased venous return to the heart, thereby decreasing left ventricular filling pressure. The effect of nitrates on the arteriolar circulation is small, and there is usually little or no change in cardiac output. Some reduction in systemic blood pressure can be seen, while there is usually no change in heart rate. In a small number of patients with myocardial infarction complicated by congestive heart failure, the use of long acting nitrates has resulted in haemodynamic and symptomatic improvement. Nitrates has also bee shown to improve variant angina. Nitrates are usually well tolerated in most patients. However, some troublesome side effects can occur, including headache, postural hypotension, and methaemoglobinaemia.

Angina Pectoris↗