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 1,117 records · Page 62Linked to original sources
PubMed1990

Intravenous isosorbide-5-mononitrate in the treatment of acute myocardial infarction.

The action of isorsorbide-5-mononitrate (IS-5-MN) infusion (range 6.0 to 10.0 mg/hour) was studied in 24 patients with and without acute heart failure (hemodynamic subsets I to IV) during acute myocardial infarction. Hemodynamic measurements were performed by right-sided cardiac catheterization. Intravenous IS-5-MN demonstrated significant hemodynamic effects compared with baseline values. In subsets I and II, a decrease in pulmonary wedge pressure (PWP) and in cardiac index (CI), without significant changes in heart rate, mean arterial pressure or systemic vascular resistance index were demonstrated. In subsets III and IV, a major increase in CI and a decrease in systemic vascular resistance index, as well as a decrease in PWP were found. Again no changes occurred in mean arterial pressure and heart rate. The dosage was similar in subsets I to IV (8.0, 7.9, 7.8 and 7.3 mg/hour); thus, the differences in the responses could not be attributed to dosage. It appears that several different patterns of hemodynamic IS-5-MN action exist, assuming that IS-5-MN operates on preload and afterload levels. The action of IS-5-MN mechanisms seems to be dependent on an initial hemodynamic subset. No patient had any deleterious hemodynamic effects. A decrease in CI in subsets I and II was not of clinical importance with these dosages. No nitrate tolerance during 9.0 hours of continuous therapy appeared.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical Trials as Topic↗
PubMed1984

Evidence for isosorbide dinitrate (ISDN) promoting effect on prostacyclin release by the lung and prostacyclin implication in ISDN-induced inhibition of platelet aggregation in humans.

We investigated thromboxane B2 (TxB2), 6-keto-PGF1 alpha (6KPGF1 alpha reflecting prostacyclin), PGE2 and PGF2 alpha plasma levels; TxB2, PGE2 and PGF2 alpha platelet production and platelet aggregation response in ascending aorta (reflecting trans-pulmonary difference) and in venous coronary sinus (reflecting transcardiac difference) simultaneously in patients with ischemic heart disease, before and after right-atrial administration of 3 mg ISDN bolus. Transcardiac differences were scarce before as well as after ISDN administration. In aortic blood, ISDN administration into the right atria resulted in a significant increase in prostacyclin and PGF2 alpha plasma levels (472% and 242%, respectively), a decrease of both PGE2 plasma level (-173%) and PGE2 platelet production (-485%) and a marked lowering of platelet aggregation response to ADP, concomittantly. In contrast, TxB2-related features were poorly affected by ISDN. In coronary sinus blood, the aortic increase in 6KPGF1 alpha and PGF2 alpha plasma levels was detected to a lower extent whereas the characteristics of platelet aggregation had returned to control levels. By contrast, PGE2 plasma level (-191%) and PGE2 platelet production (-133%) were lower than prior ISDN administration. The results we report here, strongly support the view that ISDN promotes release of prostacyclin and PGF2 alpha from the lung and inhibit PGE2 production. These prostanoids may be responsible for the concomittant platelet reactivity lowering, thus providing a basis for understanding how ISDN might relieve myocardial ischemia favoring prostanoid mediated vasodilation and inhibition of platelet reactivity.

6-Ketoprostaglandin F1 alpha↗