3 resultados para Ramipril
em Deakin Research Online - Australia
Resumo:
Objectives
Using 2 sequential studies in HOPE (Heart Outcomes Prevention Evaluation) study–type patients, the aims of this study were: 1) to test the hypothesis that ramipril improves platelet nitric oxide (NO) responsiveness: and 2) to explore biochemical and physiological effects of ramipril in a cohort selected on the basis of platelet NO resistance.
Background
Ramipril prevents cardiovascular events, but the bases for these effects remain uncertain. NO resistance at both the platelet and vascular levels is present in a substantial proportion of patients with diabetes or ischemic heart disease and is an independent risk factor for cardiovascular events.
Methods
Study 1 was a double-blind, randomized comparison of ramipril (10 mg) with placebo in a cohort of patients (n = 119) with ischemic heart disease or diabetes plus additional coronary risk factor(s), in which effects on platelet responsiveness to NO were compared. Study 2 was a subsequent short-term evaluation of the effects of ramipril in a cohort of subjects (n = 19) with impaired platelet NO responsiveness in whom additional mechanistic data were sought.
Results
In study 1, ramipril therapy increased platelet responsiveness to NO relative to the extent of aggregation (p < 0.001), but this effect occurred primarily in patients with severely impaired baseline NO responsiveness (n = 41). In study 2, ramipril also improved platelet NO responsiveness (p < 0.01), and this improvement was correlated directly with increased NO-stimulated platelet generation of cyclic guanosine monophosphate (p < 0.02) but not with changes in plasma thrombospondin-1 levels.
Conclusions
Ramipril ameliorates platelet NO resistance in HOPE study–type patients, with associated increases in soluble guanylate cyclase responsiveness to NO. This effect is likely to contribute to treatment benefit and define patients in whom ramipril therapy is particularly effective.
Resumo:
Acute myocardial infarction (M!) is the commonest cause of death in the developed countries, and it is on the rise in developing countries. Ramipril is a well-knownAngiotensin-converting enzyme (ACE) inhibitorwhich inhibits conversion ofinactive angiotensin I to active angiotensin II. Experimental studies have shown thatACE inhibitors administered chronicallybefore acuteMImight limitmyocardial infarct size, improve cardiac function and prevent cardiac hypertrophy [1, 2]. The Chinese herb, Salvia miltiorrhiza (SM), has been widely and successfully usedmainly for anginapectoris,MI and stroke [3]. Compared to ramipril, however, there is very limited biochemical information availableto demonstrate themechanismsofSMs
cardio-protective effects. This study thus investigates the possible
biochemical and molecularmechanisms ofsuch effects ofSMin Wistar rats in comparison with those oframipril.
Resumo:
In the current study, we compared purified Salvia miltiorrhiza extract (PSME) with Angiotensin-converting enzyme inhibitor, Ramipril, in in vitro experiments and also in vivo using animal model of myocardial infarction. PSME was found to have a significantly higher trolox equivalent antioxidant capacity which indicated a great capacity for scavenging free radicals. PSME could also prevent pyrogallo red bleaching and DNA damage.
After 2 weeks treatment with PSME or Ramipril, survival rates of rats with experimental myocardial infarction were marginally increased (68.2% and 71.4%) compared with saline (61.5%). The ratios of infarct size to left ventricular size in both PSME-and Ramipril-treated rats were significantly less than that in the saline-treated group. Activity of cardiac antioxidant enzyme superoxide dismutase (SOD) was significant higher while level of Thiobarbituric acid-reactive substances (TBARs) was lower in the PSME treated group. Purified and standardized Chinese herb could provide an alternative regimen for the prevention of ischemic heart disease.
