A double-blind, placebo-controlled, cross-over study was performed in 50 patients with ischemic heart disease and stable angina to determine the duration of efficacy of 8 mg molsidomine in extended-release form. Exercise testing was performed at baseline and 2, 4, 6, 8, and 10 h after intake of either the medication or the placebo. Total duration of exercise (in minutes) and total work performance (workload x min) was significantly improved in the molsidomine retard group, not only compared with baseline but also with placebo for all time-points. ST segment depression at 60 W and at maximal exercise improved similarly until 10 h after molsidomine retard treatment. The rate-pressure product (heart rate x systolic blood pressure) showed significant improvement only at 60 W. No attenuation of the obtained effects was observed after 14 days of treatment. The number of anginal attacks and the consumption of sublingual nitroderivates were significantly reduced with molsidomine retard 8 mg as compared with placebo. Molsidomine retard 8 mg is effective until at least 10 h after oral (p.o.) intake. A dose schedule of molsidomine retard 8 mg twice daily definitely reduces anginal symptoms.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1097/00005344-199504000-00008 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Antiphospholipid antibodies attenuate endothelial repair and promote neointima formation in mice.
J Am Heart Assoc
October 2014
Center for Pulmonary and Vascular Biology, Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX (V.U., W.R.L., S.K., P.W.S., C.M.).
Background: Antiphospholipid syndrome patients have antiphospholipid antibodies (aPLs) that promote thrombosis, and they have increased cardiovascular disease risk. Although the basis for the thrombosis has been well delineated, it is not known why antiphospholipid syndrome patients also have an increased prevalence of nonthrombotic vascular occlusion. The aims of this work were to determine if aPLs directly promote medial hypertrophy or neointima formation in mice and to identify the underlying mechanisms.
View Article and Find Full Text PDFElevated plasma concentration of NO and cGMP may be responsible for the decreased platelet aggregation and platelet leukocyte conjugation in platelets hypo-responsive to catecholamines.
Platelets
December 2009
Natural Products Research Institute, College of Pharmacy, Seoul National University, Seoul 151-742, Korea.
Impaired responsiveness to epinephrine and other catecholamines (CA) were previously reported in platelets of 20 approximately 30% healthy Japanese and Koreans. In the present study, the possible mechanisms of different responsiveness to CA in platelets of CA hypo-responders (CA-HY) and CA good-responders (CA-GR) were investigated. Increased platelet-leukocyte conjugate (PLC) formations were observed with whole blood of CA-GR than with that of CA-HY in both non-stimulated [mean fluorescence intensity (MFI) values: 1.
View Article and Find Full Text PDFThe neuroprotective effect of Activin A and B: implication for neurodegenerative diseases.
J Neurochem
November 2007
Eve Topf and USA National Parkinson Foundation Centers of Excellence for Neurodegenerative Diseases Research and Department of Pharmacology, Rappaport Family Research Institute, Technion-Faculty of Medicine, Haifa, Israel.
Activin is a member of the transforming growth factor-beta superfamily which comprises a growing list of multifunctional proteins that function as modulators of cell proliferation, differentiation, hormone secretion and neuronal survival. This study examined the neuroprotective effect of both Activin A and B in serum withdrawal and oxidative stress apoptotic cellular models and investigated the expression of pro- and anti-apoptotic proteins, which may account for the mechanism of Activin-induced neuroprotection. Here, we report that recombinant Activin A and B are neuroprotective against serum deprivation- and toxin- [either the parkinsonism-inducing neurotoxin, 6-hydroxydopamine (6-OHDA) or the peroxynitrite donor, 3-(4-morpholinyl) sydnonimine hydrochloride (SIN-1)] induced neuronal death in human SH-SY5Y neuroblastoma cells.
View Article and Find Full Text PDFNitric oxide and superoxide impair human placental amino acid uptake and increase Na+ permeability: implications for fetal growth.
Free Radic Biol Med
February 2004
Academic Unit of Child Health, Manchester University, St. Mary's Hospital, Manchester M13 0JH, UK.
Based on evidence that thiol and tyrosine reagents inhibit some amino acid transporters, we tested the hypothesis that NO- and O2- -derived free radicals would impair nutrient uptake by the human placenta. Syncytiotrophoblast microvillous plasma membrane vesicles (MVM) and placental villous fragments were exposed to the drug SIN-1 in the presence or absence of superoxide dismutase (SOD) and hemoglobin (Hb). The uptake of [3H]arginine, [3H]taurine, and [3H]leucine; [14C]MeAIB; and 22Na was studied in MVM, whereas the uptake of [3H]taurine was examined in villous fragments.
View Article and Find Full Text PDFAim: To compare effectiveness and tolerance of isosorbide dinitrate (ID) and molsidomin in retard forms in patients with effort angina (EA) in combination with arterial hypotension (AH).
Material And Methods: A randomised blind cross-over trial with lead-in placebo period trial compared efficiency of retard ID and molsidomin in 65 EA patients with AH (group 1) and 40 normotensive patients with coronary heart disease (group 2).
Results: Bicycle exercise has shown that retard ID and molsidomin retard were highly effective in group 1 (97% vs 92% 0 and group 2 (100 and 95%, respectively).
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!