|1.||Bayat, Gholamreza: 2 articles (09/2014 - 03/2012)|
|2.||Safari, Fatemeh: 2 articles (09/2014 - 03/2012)|
|3.||Shekarforoush, Shahnaz: 2 articles (09/2014 - 03/2012)|
|4.||Hajizadeh, Sohrab: 2 articles (09/2014 - 03/2012)|
|5.||Moghadam, Mahdi Forouzandeh: 1 article (09/2014)|
|6.||Hekmatimoghaddam, Seyedhossein: 1 article (09/2014)|
|7.||Anvari, Zahra: 1 article (09/2014)|
|8.||Cvan Trobec, Katja: 1 article (05/2014)|
|9.||Springer, Jochen: 1 article (05/2014)|
|10.||Lainscak, Mitja: 1 article (05/2014)|
06/13/1996 - "Ramiprilat attenuates hypoxia/reoxygenation injury to cardiac myocytes via a bradykinin-dependent mechanism."
09/01/1995 - "Also, when isolated neonatal rat cardiomyocytes were exposed to hypoxia/reoxygenation, ramiprilat (100 mumol/L) and bradykinin (10 nmol/L) improved cell viability (approximately 60%), and the protective effect of both agents was reversed by administration of HOE 140 (10 mumol/L). "
01/01/1991 - "In a model of standardized myocardial hypoxia (isolated working heart of the guinea pig with 30 min low flow perfusion) captopril, ramiprilat and uric acid equally improved post-hypoxic heart function. "
06/13/1996 - "The results indicate that the angiotensin-converting enzyme inhibitor ramiprilat has a protective effect on isolated cardiac myocytes exposed to hypoxia/reoxygenation and that this effect is most likely related to a local action of bradykinin on the cardiac myocyte via the activation of the kinin B2 receptor."
|2.||Myocardial Ischemia (Ischemic Heart Diseases)
07/01/2005 - "We tested the hypothesis that TK plays a protective role in myocardial ischemia by performing ischemia-reperfusion (IR) injury, with and without ischemic preconditioning (IPC) or ACE inhibitor (ramiprilat) pretreatment, in vivo in littermate wild-type (WT) or TK-deficient (TK-/-) mice. "
03/01/2012 - "HYPOTHESIS/INTRODUCTION: Our aim was to investigate whether a non-hypotensive dose of ramiprilat and losartan has myocardial protective effects during myocardial ischemia/reperfusion in vivo. "
09/01/2014 - "The aim of this study was to investigate the early changes of cardiac uncoupling protein-2 (UCP2) expression following myocardial ischemia reperfusion in rats chronically treated with ramiprilat and losartan. "
09/01/2014 - "Expressional profile of cardiac uncoupling protein-2 following myocardial ischemia reperfusion in losartan- and ramiprilat-treated rats."
09/01/1994 - "Ramiprilat, the nitric oxide synthase inhibitor NG-nitro-L-NAME (L-NAME), ramiprilat plus L-NAME, or saline (n = 8 each group), were administered i.v. in intact animal preparations of experimentally induced acute myocardial ischemia. "
08/01/1994 - "In isolated working rat hearts, perfusion with ramiprilat (10 nM to 10 microM) reduced the incidence and duration of ventricular fibrillation, and improved cardiodynamics and myocardial metabolism. "
10/01/1999 - "Apstatin and ramiprilat also significantly reduced the duration of reperfusion-induced ventricular fibrillation by 69 and 61%, respectively. "
12/01/1988 - "In ischaemic working rat heart preparations perfusion with ramiprilat (2.58 x 10(-7) mol/l) or single oral pretreatment with ramipril (1 mg/kg) protected the heart from the ventricular fibrillations that invariably occurred upon reperfusion after ischaemia. "
01/01/1986 - "In ischemic isolated rat hearts, both single oral pretreatment with ramipril (1 mg/kg) or perfusion with the active moiety, ramiprilat (10 micrograms/ml), protected against ventricular fibrillation, which invariably occurred in control hearts during reperfusion. "
01/01/1987 - "In ischemic isolated rat hearts, perfusion with ramiprilat (100 ng/ml, 2.58 x 10(-7) mol/l), the active moiety of the CE inhibitor ramipril, after coronary occlusion protected against ventricular fibrillation that invariably occurred in untreated control hearts in the reperfusion period. "
|4.||Ventricular Premature Complexes (Premature Ventricular Contraction)
10/01/1996 - "We observed (1) in hearts treated with ramiprilat (100 nmol/L) or captopril (5 mumol/L), a significant reduction of ET-1 secretion under all three experimental conditions and fewer ventricular extrasystoles during reperfusion; (2) increased ET-1 secretion and numerous tachyarrhythmic events in the presence of ACE inhibitor and a bradykinin B2 receptor antagonist, icatibant (100 nmol/L); (3) an almost-complete suppression of reperfusion arrhythmias when an ET receptor antagonist, ie, SB 209670 (5 mumol/L) or PD 142893 (200 nmol/L), was infused together with ACE inhibitor and icatibant; and (4) SB 209670 alone to be equally antiarrhythmic as ACE inhibitors. "
03/28/2003 - "These data indicate that administration of saralasin but not ramiprilat could be protective against acute pancreatitis and that activation of pancreatic RAS in acute pancreatitis may play a role in pancreatic tissue injury."
03/28/2003 - "However, the same recipe of ramiprilat, a specific inhibitor for angiotensin-converting enzyme, at a dose of 20 microg/kg did not provide any protective effect against acute pancreatitis. "
03/28/2003 - "Differential effects of saralasin and ramiprilat, the inhibitors of renin-angiotensin system, on cerulein-induced acute pancreatitis."
|5.||Angiotensin-Converting Enzyme Inhibitors (ACE Inhibitors)
|6.||Bradykinin B2 Receptor
|7.||Uric Acid (Urate)
|8.||Saralasin (Saralasin Acetate)