The Experts below are selected from a list of 11334 Experts worldwide ranked by ideXlab platform
Norbert F. Voelkel - One of the best experts on this subject based on the ideXlab platform.
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treatment of severe pulmonary hypertension a bradykinin receptor 2 agonist b9972 causes reduction of pulmonary artery pressure and Right Ventricular Hypertrophy
Peptides, 2005Co-Authors: Laimute Tarasevicienestewart, Robertas Scerbavicius, John M Stewart, Lajos Gera, Yoshiki Demura, Carlyne D Cool, Michael Kasper, Norbert F. VoelkelAbstract:Abstract Bradykinin is an important modulator of endothelial cell function and has also a powerful cardioprotective effect. Here we report that treatment of severely pulmonary hypertensive rats (that recapitulate several of the physiological and pathological characteristics of the human pulmonary vascular disease, including dramatic Right Ventricular Hypertrophy, pericardial effusion and death) with a newly synthesized long-acting bradykinin B2 receptor agonist B9972 caused reduction of the pulmonary artery pressure (PAP = 51 ± 2.0 versus 68 ± 2.8 of untreated animals) and of Right Ventricular Hypertrophy (Rv/Lv + S = 0.55 ± 0.02 versus 0.73 ± 0.03 of untreated rats) and activation of Akt. Long-term stimulation with B9972 in our animal model of SPH resulted in decreased expression of the B2 receptor in lung vasculature. Treatment with B9972 decreased the number of plexiform lesions in the lungs by inducing cell apoptosis in the obliterated vessels and by restoring caveolin-1 expression. B9972 also promoted eNOS activation. In vitro B9972 caused activation of caspase-3 as well as Erk and induction of prostacyclin production in rat pulmonary microvascular EC. Taken together our data suggest that a stable bradykinin B2 agonist B9972 demonstrates the capacity to reduce severe pulmonary hypertension, Right Ventricular Hypertrophy and induce apoptosis of hyperproliferative cells in pre-capillary pulmonary arterioles.
Laimute Tarasevicienestewart - One of the best experts on this subject based on the ideXlab platform.
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treatment of severe pulmonary hypertension a bradykinin receptor 2 agonist b9972 causes reduction of pulmonary artery pressure and Right Ventricular Hypertrophy
Peptides, 2005Co-Authors: Laimute Tarasevicienestewart, Robertas Scerbavicius, John M Stewart, Lajos Gera, Yoshiki Demura, Carlyne D Cool, Michael Kasper, Norbert F. VoelkelAbstract:Abstract Bradykinin is an important modulator of endothelial cell function and has also a powerful cardioprotective effect. Here we report that treatment of severely pulmonary hypertensive rats (that recapitulate several of the physiological and pathological characteristics of the human pulmonary vascular disease, including dramatic Right Ventricular Hypertrophy, pericardial effusion and death) with a newly synthesized long-acting bradykinin B2 receptor agonist B9972 caused reduction of the pulmonary artery pressure (PAP = 51 ± 2.0 versus 68 ± 2.8 of untreated animals) and of Right Ventricular Hypertrophy (Rv/Lv + S = 0.55 ± 0.02 versus 0.73 ± 0.03 of untreated rats) and activation of Akt. Long-term stimulation with B9972 in our animal model of SPH resulted in decreased expression of the B2 receptor in lung vasculature. Treatment with B9972 decreased the number of plexiform lesions in the lungs by inducing cell apoptosis in the obliterated vessels and by restoring caveolin-1 expression. B9972 also promoted eNOS activation. In vitro B9972 caused activation of caspase-3 as well as Erk and induction of prostacyclin production in rat pulmonary microvascular EC. Taken together our data suggest that a stable bradykinin B2 agonist B9972 demonstrates the capacity to reduce severe pulmonary hypertension, Right Ventricular Hypertrophy and induce apoptosis of hyperproliferative cells in pre-capillary pulmonary arterioles.
Shaul G Massry - One of the best experts on this subject based on the ideXlab platform.
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excess pth in crf induces pulmonary calcification pulmonary hypertension and Right Ventricular Hypertrophy
Kidney International, 1995Co-Authors: Mohammad Akmal, Robert Barndt, Azizullah N Ansari, John G Mohler, Shaul G MassryAbstract:Excess PTH in CRF induces pulmonary calcification, pulmonary hypertension and Right Ventricular Hypertrophy. Calcification of the lungs occurs in chronic renal failure (CRF) and may adversely affect both pulmonary and Right Ventricular function. The present study examined the role of excess parathyroid hormone (PTH) in the genesis of pulmonary calcifications in dogs with experimental CRF and evaluated calcium content of lungs, diffusing lung capacity (DCO), mean pulmonary artery pressure (MPAP), Right Ventricular pressure (RVP), and Right Ventricular Hypertrophy (RVH) in six normal, six with CRF, and six thyroparathyroidectomized (CRF-PTX) dogs. CRF-PTX animals were maintained normocalcemic and euthyroid. The degree and duration of CRF were not different between the two groups with CRF. The mean value of the serum PTH in CRF dogs was 166 ± 42 µlEq/ml, but was undetectable in CRF-PTX animals. Thallium scan provided evidence consistent with RVH in CRF dogs but not in CRF-PTX animals. Calcium content of lungs was markedly elevated in CRF dogs (7656 ± 1657 mg/kg dry wt) but modestly increased in CRF-PTX (1057 ± 117 mg/kg dry wt) as compared to normal (673 ± 34 mg/kg dry wt). RVP and MPAP were significantly (P
Steven M Kawut - One of the best experts on this subject based on the ideXlab platform.
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validity of the surface electrocardiogram criteria for Right Ventricular Hypertrophy
Journal of the American College of Cardiology, 2014Co-Authors: Isaac R Whitman, Vickas V Patel, Elsayed Z Soliman, David A Bluemke, Amy Praestgaard, Aditya Jain, David M Herrington, Joao A C Lima, Steven M KawutAbstract:Objectives: The study aimed to assess the diagnostic properties of electrocardiographic (ECG) criteria for Right Ventricular Hypertrophy (RVH) measured by cardiac magnetic resonance imaging (cMRI) ...
Robertas Scerbavicius - One of the best experts on this subject based on the ideXlab platform.
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treatment of severe pulmonary hypertension a bradykinin receptor 2 agonist b9972 causes reduction of pulmonary artery pressure and Right Ventricular Hypertrophy
Peptides, 2005Co-Authors: Laimute Tarasevicienestewart, Robertas Scerbavicius, John M Stewart, Lajos Gera, Yoshiki Demura, Carlyne D Cool, Michael Kasper, Norbert F. VoelkelAbstract:Abstract Bradykinin is an important modulator of endothelial cell function and has also a powerful cardioprotective effect. Here we report that treatment of severely pulmonary hypertensive rats (that recapitulate several of the physiological and pathological characteristics of the human pulmonary vascular disease, including dramatic Right Ventricular Hypertrophy, pericardial effusion and death) with a newly synthesized long-acting bradykinin B2 receptor agonist B9972 caused reduction of the pulmonary artery pressure (PAP = 51 ± 2.0 versus 68 ± 2.8 of untreated animals) and of Right Ventricular Hypertrophy (Rv/Lv + S = 0.55 ± 0.02 versus 0.73 ± 0.03 of untreated rats) and activation of Akt. Long-term stimulation with B9972 in our animal model of SPH resulted in decreased expression of the B2 receptor in lung vasculature. Treatment with B9972 decreased the number of plexiform lesions in the lungs by inducing cell apoptosis in the obliterated vessels and by restoring caveolin-1 expression. B9972 also promoted eNOS activation. In vitro B9972 caused activation of caspase-3 as well as Erk and induction of prostacyclin production in rat pulmonary microvascular EC. Taken together our data suggest that a stable bradykinin B2 agonist B9972 demonstrates the capacity to reduce severe pulmonary hypertension, Right Ventricular Hypertrophy and induce apoptosis of hyperproliferative cells in pre-capillary pulmonary arterioles.
