Browsing by Autor "Carlos Salinas Salmón"

Now showing 1 - 12 of 12

Exaggerated Pulmonary Hypertension and Right Ventricular Dysfunction in High-Altitude Dwellers With Patent Foramen Ovale
(Elsevier BV, 2014) Roman Brenner; Lorenza Pratali; Stefano F. Rimoldi; Carla Ximena Murillo Jauregui; Rodrigo Soria; Emrush Rexhaj; Carlos Salinas Salmón; Mercedes Villena; Catherine Romero; Cláudio Sartori
Exaggerated Pulmonary Hypertension During Mild Exercise in Chronic Mountain Sickness
(Elsevier BV, 2009) Thomas Stüber; Cláudio Sartori; Marcos Schwab; Pierre‐Yves Jayet; Stefano F. Rimoldi; Sophie Garcin; Sébastien Thalmann; Hilde Spielvogel; Carlos Salinas Salmón; Mercedes Villena
Exercise Induces Rapid Interstitial Lung Water Accumulation in Patients With Chronic Mountain Sickness
(Elsevier BV, 2011) Lorenza Pratali; Stefano F. Rimoldi; Emrush Rexhaj; Damian Hutter; Francesco Faita; Carlos Salinas Salmón; Mercedes Villena; Rosa Sicari; Eugenio Picano; Yves Allemann
Increasing respiratory dead space improves sleep disordered breathing and hypoxemia in patients with chronic mountain sickness
(Wiley, 2011) Emrush Rexhaj; Stefano F. Rimoldi; Pierre‐Yves Jayet; Alban Lovis; Daniela Andries; Carlos Salinas Salmón; Mercedes Villena; Yves Allemann; Raphaël Heinzer; Raphaël Heinzer
Chronic mountain sickness (CMS) is a major public health problem characterized by chronic hypoxemia and erythrocytosis. The underlying mechanism is unknown. Sleep disordered breathing (SDB) is frequent at high altitude. We recently found that increasing the respiratory dead space markedly improves SDB in mountaineers. We speculated that this procedure also has beneficial effects in CMS patients. To test this hypothesis, in 17 male Bolivian high-altitude dwellers (56±9 y) suffering from CMS full night sleep recordings were obtained in random order during one night spent with and one without a 500 ml increase in respiratory dead space through a custom designed full face mask. Recordings were also obtained in 6 control subjects. The major new findings were two-fold; a) CMS patients present markedly more severe SDB and hypoxemia (P<.01) than control subjects; and b) added dead space dramatically improved SDB in CMS patients, as evidenced by a decrease of the apnea/hypopnea (P<.01), hypopnea (P=.01) and oxygen desaturation (P<.01) indexes, and an increase of the nocturnal oxygen saturation (P=.01). The procedure was well tolerated. Here, we show for the first time that increasing respiratory dead space dramatically improves SDB in patients with CMS. We speculate that its long-term use will improve erythrocytosis and pulmonary hypertension and offer an inexpensive treatment for this major public health problem.
Novel Insights into Cardiovascular Regulation in Patients with Chronic Mountain Sickness
(Springer Nature, 2016) Stefano F. Rimoldi; Emrush Rexhaj; Mercedes Villena; Carlos Salinas Salmón; Yves Allemann; Urs Scherrer; Cláudio Sartori
Oxidative-Nitrosative Stress and Systemic Vascular Function in Highlanders With and Without Exaggerated Hypoxemia
(Elsevier BV, 2013) Damian M. Bailey; Stefano F. Rimoldi; Emrush Rexhaj; Lorenza Pratali; Carlos Salinas Salmón; Mercedes Villena; Jane McEneny; Ian Young; Pascal Nicod; Yves Allemann
Perinatal hypoxia increases susceptibility to high-altitude polycythemia and attendant pulmonary vascular dysfunction
(American Physical Society, 2015) Colleen G. Julian; Marcelino Gonzales; Armando Rodríguez; Diva Bellido; Carlos Salinas Salmón; Anne Ladenburger; Lindsay Reardon; Enrique Vargas; Lorna G. Moore
Perinatal exposures exert a profound influence on physiological function, including developmental processes vital for efficient pulmonary gas transfer throughout the lifespan. We extend the concept of developmental programming to chronic mountain sickness (CMS), a debilitating syndrome marked by polycythemia, ventilatory impairment, and pulmonary hypertension that affects ∼10% of male high-altitude residents. We hypothesized that adverse perinatal oxygenation caused abnormalities of ventilatory and/or pulmonary vascular function that increased susceptibility to CMS in adulthood. Subjects were 67 male high-altitude (3,600-4,100 m) residents aged 18-25 yr with excessive erythrocytosis (EE, Hb concentration ≥18.3 g/dl), a preclinical form of CMS, and 66 controls identified from a community-based survey (n = 981). EE subjects not only had higher Hb concentrations and erythrocyte counts, but also lower alveolar ventilation, impaired pulmonary diffusion capacity, higher systolic pulmonary artery pressure, lower pulmonary artery acceleration time, and more frequent right ventricular hypertrophy, than controls. Compared with controls, EE subjects were more often born to mothers experiencing hypertensive complications of pregnancy and hypoxia during the perinatal period, with each increasing the risk of developing EE (odds ratio = 5.25, P = 0.05 and odds ratio = 6.44, P = 0.04, respectively) after other factors known to influence EE status were taken into account. Adverse perinatal oxygenation is associated with increased susceptibility to EE accompanied by modest abnormalities of the pulmonary circulation that are independent of increased blood viscosity. The association between perinatal hypoxia and EE may be due to disrupted alveolarization and microvascular development, leading to impaired gas exchange and/or pulmonary hypertension.
Pulmonary Hypertension in High-Altitude Dwellers: Novel Mechanisms, Unsuspected Predisposing Factors
(Springer Nature, 2007) Urs Scherrer; Pierre Turini; Sébastien Thalmann; Damian Hutter; Carlos Salinas Salmón; Thomas Stüber; Sidney Shaw; Pierre -Yves Jayet; Céline Sartori-Cucchia; Mercedes Villena
Respiratory Nitric Oxide and Pulmonary Artery Pressure in Children of Aymara and European Ancestry at High Altitude
(Elsevier BV, 2008) Thomas Stüber; Cláudio Sartori; Carlos Salinas Salmón; Damian Hutter; Sébastien Thalmann; Pierre Turini; Pierre‐Yves Jayet; Marcos Schwab; Céline Sartori-Cucchia; Mercedes Villena
RV Contractility and Exercise-Induced Pulmonary Hypertension in Chronic Mountain Sickness
(Elsevier BV, 2013) Lorenza Pratali; Yves Allemann; Stefano F. Rimoldi; Francesco Faita; Damian Hutter; Emrush Rexhaj; Roman Brenner; Damian M. Bailey; Cláudio Sartori; Carlos Salinas Salmón
Systemic Vascular Dysfunction in Patients With Chronic Mountain Sickness
(Elsevier BV, 2011) Stefano F. Rimoldi; Emrush Rexhaj; Lorenza Pratali; Damian M. Bailey; Damian Hutter; Francesco Faita; Carlos Salinas Salmón; Mercedes Villena; Pascal Nicod; Yves Allemann
Unique DNA Methylation Patterns in Offspring of Hypertensive Pregnancy
(Wiley, 2015) Colleen G. Julian; Brent S. Pedersen; Carlos Salinas Salmón; Ivana V. Yang; Marcelino Gonzales; Enrique Vargas; Lorna G. Moore; David A. Schwartz
Epigenomic processes are believed to play a pivotal role for the effect of environmental exposures in early life to modify disease risk throughout the lifespan. Offspring of women with hypertensive complications of pregnancy (HTNPREG ) have an increased risk of developing systemic and pulmonary vascular dysfunction in adulthood. In this preliminary report, we sought to determine whether epigenetic modifications of genes involved in the regulation of vascular function were present in HTNPREG offspring. We contrasted DNA methylation and gene expression patterns of peripheral blood mononuclear cells obtained from young male offspring of HTNPREG (n = 5) to those of normotensive controls (n = 19). In HTNPREG offspring we identified six differentially methylated regions (DMRs) including three genes (SMOC2, ARID1B and CTRHC1) relevant to vascular function. The transcriptional activity of ARID1B and CTRCH1 was inversely related to methylation status. HTNPREG offspring had higher systolic pulmonary artery pressure (sPPA ) versus controls. Our findings demonstrate that epigenetic marks are altered in offspring of HTNPREG with a modest elevation of sPPA and introduce novel epigenomic targets for further study. On the basis of these findings we speculate that epigenomic mechanisms may be involved in mediating the effect of HTNPREG to raise the risk of vascular disease later in life.