|1.||Stasch, Johannes-Peter: 11 articles (01/2015 - 07/2006)|
|2.||Radovits, Tamás: 5 articles (10/2015 - 08/2009)|
|3.||Szabó, Gábor: 5 articles (10/2015 - 08/2009)|
|4.||Frey, Reiner: 5 articles (11/2012 - 12/2008)|
|5.||Karck, Matthias: 4 articles (10/2015 - 08/2009)|
|6.||Loganathan, Sivakkanan: 3 articles (10/2015 - 08/2009)|
|7.||Hirschberg, Kristóf: 3 articles (10/2015 - 08/2009)|
|8.||Brouckaert, Peter: 3 articles (06/2015 - 01/2013)|
|9.||Gheorghiade, Mihai: 3 articles (01/2013 - 12/2009)|
|10.||Korkmaz, Sevil: 3 articles (01/2013 - 08/2009)|
01/01/2009 - "The sGC activator BAY 58-2667 has demonstrated efficacy in a proof-of-concept study in patients with acute decompensated heart failure (ADHF), reducing pre- and afterload and increasing cardiac output from baseline. "
01/01/2013 - "This study evaluated the haemodynamic effect and safety of cinaciguat added to standard therapy in patients with acute decompensated heart failure (ADHF). "
12/01/2009 - "Preliminary studies of cinaciguat in patients with acute decompensated heart failure show substantial improvements in haemodynamics and symptoms, whilst maintaining renal function."
11/01/2012 - "Cinaciguat is intended for use in patients with acute decompensated heart failure. "
08/01/2012 - "In conclusion, cinaciguat, a promising drug candidate for the treatment of acute decompensated heart failure, will not require dose adjustment based on renal function."
|2.||Hypotension (Low Blood Pressure)
01/01/2013 - "No adverse effects on the 30-day mortality were seen; however, the trial was stopped prematurely due to an increased occurrence of hypotension at cinaciguat doses ≥200 µg/h. "
11/01/2014 - "In vehicle controls (n=3), in which cinaciguat-induced hypotension was mimicked by aortic compression, the NOS inhibition-induced changes were not affected. "
06/02/2009 - "Cinaciguat was well tolerated, with 13 of 60 patients reporting 14 drug-related treatment-emergent adverse events of mild to moderate intensity, most commonly hypotension. "
01/01/2015 - "The haemodynamic effects of NO are abolished, but those of the sGC activator cinaciguat are enhanced in apo-sGC mice, suggesting that the effects of NO on smooth muscle relaxation, blood pressure regulation and inhibition of platelet aggregation require sGC activation by NO. Tumour necrosis factor (TNF)-induced hypotension and mortality are preserved in apo-sGC mice, indicating that pathways other than sGC signalling mediate the cardiovascular collapse in shock. "
09/01/2012 - "Cinaciguat (BAY 58-2667) is a soluble guanylate cyclase (sGC) activator that, in a previous study among patients with acute heart failure syndromes (AHFS), improved pulmonary capillary wedge pressure (PCWP) at the expense of significant hypotension at doses ≥200 µg/h. "
03/15/2012 - "Primary adult mouse cardiomyocytes were isolated and treated with cinaciguat before simulated ischemia/reoxygenation. "
08/25/2009 - "A cardioprotective effect of postischemic cinaciguat treatment was shown in a canine model of global ischemia/reperfusion. "
10/01/2015 - "Cinaciguat also significantly decreased myocardial DNA strand breaks induced by ischemia/reperfusion during transplantation and reduced death of cardiomyocytes in a cellular model of oxidative stress. "
03/15/2012 - "We tested the hypothesis that cinaciguat might trigger protection against ischemia/reperfusion (I/R) in the heart and adult cardiomyocytes through cGMP/protein kinase G (PKG)-dependent generation of hydrogen sulfide (H(2)S). "
01/01/2015 - "Since hydrogen sulfide (H2S) has been implicated in mediating the cardioprotective effects of the cGMP modulators tadalafil and cinaciguat, we tested the hypothesis that myocardial gene therapy with PKG exerts cardioprotection against ischemia/reperfusion (I/R) injury through a mechanism involving H2S. "
|4.||Pulmonary Hypertension (Ayerza Syndrome)
11/01/2011 - "We speculate that increased NO-insensitive sGC may contribute to the pathogenesis of PPHN, and cinaciguat may provide a novel treatment of severe pulmonary hypertension."
11/01/2011 - "To determine whether altered sGC expression or activity due to oxidized sGC contributes to high pulmonary vascular resistance (PVR) and poor NO responsiveness, we studied the effects of cinaciguat (BAY 58-2667), an sGC activator, on pulmonary artery smooth muscle cells (PASMC) from normal fetal sheep and sheep exposed to chronic intrauterine pulmonary hypertension (i.e., PPHN). "
08/01/2009 - "We conclude that cinaciguat causes potent and sustained fetal pulmonary vasodilation that is augmented in the presence of oxidized sGC and speculate that cinaciguat may have therapeutic potential for severe neonatal pulmonary hypertension."
11/01/2011 - "Cinaciguat, a soluble guanylate cyclase activator, augments cGMP after oxidative stress and causes pulmonary vasodilation in neonatal pulmonary hypertension."
|5.||Myocardial Ischemia (Ischemic Heart Diseases)
|1.||Guanylate Cyclase (Guanylyl Cyclase)
|2.||Hydrogen Sulfide (Sulfide, Hydrogen)
|3.||Cyclooxygenase 2 (Cyclooxygenase-2)
|4.||Cyclic GMP-Dependent Protein Kinases (Protein Kinase G)
|5.||Transforming Growth Factor beta (TGF-beta)
|6.||Messenger RNA (mRNA)
|8.||Actins (F Actin)
|2.||Transplantation (Transplant Recipients)
|3.||Cardiopulmonary Bypass (Heart-Lung Bypass)