Browsing by Autor "Carlos E. Salinas"

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Acute and Chronic Altitude-Induced Cognitive Dysfunction in Children and Adolescents
(Elsevier BV, 2015) Stefano F. Rimoldi; Emrush Rexhaj; Hervé Duplain; Sébastien Urben; Joël Billieux; Yves Allemann; Catherine Romero; Alejandro Ayaviri; Carlos E. Salinas; Mercedes Villena
Acute hypoxia‐reoxygenation and vascular oxygen sensing in the chicken embryo
(Wiley, 2017) Riazuddin Mohammed; Carlos E. Salinas; Dino A. Giussani; Carlos E. Blanco; Ángel Cogolludo; Eduardo Villamor
Fetal/perinatal hypoxia is one of the most common causes of perinatal morbidity and mortality and is frequently accompannied by vascular dysfunction. However, the mechanisms involved have not been fully delineated. We hypothesized that exposure to acute hypoxia-reoxygenation induces alterations in vascular O2 sensing/signaling as well as in endothelial function in the chicken embryo pulmonary artery (PA), mesenteric artery (MA), femoral artery (FA), and ductus arteriosus (DA). Noninternally pipped 19-day embryos were exposed to 10% O2 for 30 min followed by reoxygenation with 21% O2 or 80% O2 Another group was constantly maintained at 21% O2 or at 21% O2 for 30 min and then exposed to 80% O2 Following treatment, responses of isolated blood vessels to hypoxia as well as endothelium-dependent (acetylcholine) and -independent (sodium nitroprusside and forskolin) relaxation were investigated in a wire myograph. Hypoxia increased venous blood lactate from 2.03 ± 0.18 to 15.98 ± 0.73 mmol/L (P < 0.001) and reduced hatchability to 0%. However, ex vivo hypoxic contraction of PA and MA, hypoxic relaxation of FA, and normoxic contraction of DA were not significantly different in any of the experimental groups. Relaxations induced by acetylcholine, sodium nitroprusside, and forskolin in PA, MA, FA, and DA rings were also similar in the four groups. In conclusion, exposure to acute hypoxia-reoxygenation did not affect vascular oxygen sensing or reactivity in the chicken embryo. This suggests that direct effects of acute hypoxia-reoxygenation on vascular function does not play a role in the pathophysiology of hypoxic cardiovascular injury in the perinatal period.
Adrenocortical Suppression in Highland Chick Embryos Is Restored during Incubation at Sea Level
(Mary Ann Liebert, Inc., 2011) Carlos E. Salinas; Mercedes Villena; Carlos E. Blanco; Dino A. Giussani
By combining the chick embryo model with incubation at high altitude, this study tested the hypothesis that development at high altitude is related to a fetal origin of adrenocortical but not adrenomedullary suppression and that hypoxia is the mechanism underlying the relationship. Fertilized eggs from sea-level or high altitude hens were incubated at sea level or high altitude. Fertilized eggs from sea-level hens were also incubated at altitude with oxygen supplementation. At day 20 of incubation, embryonic blood was taken for measurement of plasma corticotropin, corticosterone, and Po(2). Following biometry, the adrenal glands were collected and frozen for measurement of catecholamine content. Development of chick embryos at high altitude led to pronounced adrenocortical blunting, but an increase in adrenal catecholamine content. These effects were similar whether the fertilized eggs were laid by sea-level or high altitude hens. The effects of high altitude on the stress axes were completely prevented by incubation at high altitude with oxygen supplementation. When chick embryos from high altitude hens were incubated at sea level, plasma hormones and adrenal catecholamine content were partially restored toward levels measured in sea-level chick embryos. There was a significant correlation between adrenocortical blunting and elevated adrenal catecholamine content with both asymmetric growth restriction and fetal hypoxia. The data support the hypothesis tested and provide evidence to isolate the direct contribution of developmental hypoxia to alterations in the stress system.
Cardiac and vascular disease prior to hatching in chick embryos incubated at high altitude
(Cambridge University Press, 2009) Carlos E. Salinas; C. E. Blanco; Mercedes Villena; Emily J. Camm; J. D. Tuckett; Ruwan Weerakkody; Andrew D. Kane; A.M. Shelley; F. B. P. Wooding; Mai Trinh Quy
The partial contributions of reductions in fetal nutrition and oxygenation to slow fetal growth and a developmental origin of cardiovascular disease remain unclear. By combining high altitude with the chick embryo model, we have previously isolated the direct effects of high-altitude hypoxia on growth. This study isolated the direct effects of high-altitude hypoxia on cardiovascular development. Fertilized eggs from sea-level or high-altitude hens were incubated at sea level or high altitude. Fertilized eggs from sea-level hens were also incubated at high altitude with oxygen supplementation. High altitude promoted embryonic growth restriction, cardiomegaly and aortic wall thickening, effects which could be prevented by incubating eggs from high-altitude hens at sea level or by incubating eggs from sea-level hens at high altitude with oxygen supplementation. Embryos from high-altitude hens showed reduced effects of altitude incubation on growth restriction but not on cardiovascular remodeling. The data show that: (1) high-altitude hypoxia promotes embryonic cardiac and vascular disease already evident prior to hatching and that this is associated with growth restriction; (2) the effects can be prevented by increased oxygenation; and (3) the effects are different in embryos from sea-level or high-altitude hens.
Exaggerated exercise‐induced pulmonary vasoconstriction in reentry pulmonary edema‐prone subjects and in offspring of preeclampsia
(Wiley, 2007) Cláudio Sartori; Thomas Stüber; Marcos Schwab; Pierre‐Yves Jayet; Jonathan Bloch; Sébastien Thalmann; Hilde Spielvogel; Carlos E. Salinas; Mercedes Villena; Urs Scherrer
Offspring of mothers suffering from preeclampsia and subjects with a history of reentry high‐altitude pulmonary edema (re‐entry HAPE) display sustained hypoxic pulmonary hypertension when living at high altitude and a predisposition to pulmonary edema. The underlying mechanisms are unknown. We hypothesized that the predisposition to pulmonary edema could be caused by capillary stress failure related to exaggerated pulmonary hypertension. We, therefore, estimated the pulmonary artery pressure response (Doppler echocardiography) to mild exercise in 18 re‐entry HAPE‐prone subjects, 12 offspring of preeclampsia and 29 controls, all born and living in La Paz, Bolivia (3600 m). As expected, mean±SD systolic pulmonary artery pressure at rest was higher in re‐entry HAPE prone subjects and offspring of preeclampsia than in controls (42±7 and 37±8 vs. 30±7 mm Hg, P<0.001). Most importantly, the exercise‐induced increase in pulmonary artery pressure was 50 percent larger in the two groups of subjects at risk than in controls (21±8 and 21±10 vs. 14±7 mm Hg, P=0.02). These data provide the first evidence for a markedly exaggerated pulmonary vasoconstrictor response to exercise in high altitude dwellers known to have an augmented susceptibility to develop pulmonary edema. We speculate that this exaggerated response may predispose them to pulmonary edema by causing capillary stress failure.
High altitude hypoxia and blood pressure dysregulation in adult chickens
(Cambridge University Press, 2012) Emilio A. Herrera; Carlos E. Salinas; C. E. Blanco; Mercedes Villena; Dino A. Giussani
Although it is accepted that impaired placental perfusion in complicated pregnancy can slow fetal growth and programme an increased risk of cardiovascular dysfunction at adulthood, the relative contribution of reductions in fetal nutrition and in fetal oxygenation as the triggering stimulus remains unclear. By combining high altitude (HA) with the chick embryo model, we have previously isolated the direct effects of HA hypoxia on embryonic growth and cardiovascular development before hatching. This study isolated the effects of developmental hypoxia on cardiovascular function measured in vivo in conscious adult male and female chickens. Chick embryos were incubated, hatched and raised at sea level (SL, nine males and nine females) or incubated, hatched and raised at HA (seven males and seven females). At 6 months of age, vascular catheters were inserted under general anaesthesia. Five days later, basal blood gas status, basal cardiovascular function and cardiac baroreflex responses were investigated. HA chickens had significantly lower basal arterial PO2 and haemoglobin saturation, and significantly higher haematocrit than SL chickens, independent of the sex of the animal. HA chickens had significantly lower arterial blood pressure than SL chickens, independent of the sex of the animal. Although the gain of the arterial baroreflex was decreased in HA relative to SL male chickens, it was increased in HA relative to SL female chickens. We show that development at HA lowers basal arterial blood pressure and alters baroreflex sensitivity in a sex-dependent manner at adulthood.
High-Altitude Hypoxia and Echocardiographic Indices of Pulmonary Hypertension in Male and Female Chickens at Adulthood
(Japanese Circulation Society, 2014) Carlos E. Salinas; Carlos E. Blanco; Mercedes Villena; Dino A. Giussani
The data show that chronic hypoxia during development at HA is associated with echocardiocraphic indices of pulmonary hypertension at adulthood in a highly sex-dependent manner.
Preeclampsia and risk of maternal pulmonary hypertension at high altitude in Bolivia
(Cambridge University Press, 2023) Carlos E. Salinas; Olga Patey; Clara Murillo; Marcelino Gonzales; V. Espinoza; S. Mendoza; R. Ruı́z; Rodrigo Vargas; Yalile Perez; Juan José Montaño Moreno
Women with a history of preeclampsia (PE) have a greater risk of pulmonary arterial hypertension (PAH). In turn, pregnancy at high altitude is a risk factor for PE. However, whether women who develop PE during highland pregnancy are at risk of PAH before and after birth has not been investigated. We tested the hypothesis that during highland pregnancy, women who develop PE are at greater risk of PAH compared to women undergoing healthy highland pregnancies. The study was on 140 women in La Paz, Bolivia (3640m). Women undergoing healthy highland pregnancy were controls (C, n = 70; 29 ± 3.3 years old, mean±SD). Women diagnosed with PE were the experimental group (PE, n = 70, 31 ± 2 years old). Conventional (B- and M-mode, PW Doppler) and modern (pulsed wave tissue Doppler imaging) ultrasound were applied for cardiovascular íííassessment. Spirometry determined maternal lung function. Assessments occurred at 35 ± 4 weeks of pregnancy and 6 ± 0.3 weeks after birth. Relative to highland controls, highland PE women had enlarged right ventricular (RV) and right atrial chamber sizes, greater pulmonary artery dimensions and increased estimated RV contractility, pulmonary artery pressure and pulmonary vascular resistance. Highland PE women had lower values for peripheral oxygen saturation, forced expiratory flow and the bronchial permeability index. Differences remained 6 weeks after birth. Therefore, women who develop PE at high altitude are at greater risk of PAH before and long after birth. Hence, women with a history of PE at high altitude have an increased cardiovascular risk that transcends the systemic circulation to include the pulmonary vascular bed.
Preeclampsia and Risk of Maternal Pulmonary Hypertension at High Altitude in Bolivia
(RELX Group (Netherlands), 2022) Carlos E. Salinas; Olga Patey; Carla Victoria Jara Murillo; Marcelino Gonzales; Vania Espinoza; Silvia Mendoza; Rosario Ruiz; Rodrigo Vargas; Yuri Vázquez Pérez; Jaime Montaño
Pulmonary-Artery Pressure and Exhaled Nitric Oxide in Bolivian and Caucasian High Altitude Dwellers
(Mary Ann Liebert, Inc., 2008) Marcos Schwab; Pierre‐Yves Jayet; Thomas Stüber; Carlos E. Salinas; Jonathan Bloch; Hilde Spielvogel; Mercedes Villena; Yves Allemann; Cláudio Sartori; Urs Scherrer
There is evidence that high altitude populations may be better protected from hypoxic pulmonary hypertension than low altitude natives, but the underlying mechanism is incompletely understood. In Tibetans, increased pulmonary respiratory NO synthesis attenuates hypoxic pulmonary hypertension. It has been speculated that this mechanism may represent a generalized high altitude adaptation pattern, but direct evidence for this speculation is lacking. We therefore measured systolic pulmonary-artery pressure (Doppler chocardiography) and exhaled nitric oxide (NO) in 34 healthy, middle-aged Bolivian high altitude natives and in 34 age- and sex-matched, well-acclimatized Caucasian low altitude natives living at high altitude (3600 m). The mean+/-SD systolic right ventricular to right atrial pressure gradient (24.3+/-5.9 vs. 24.7+/-4.9 mmHg) and exhaled NO (19.2+/-7.2 vs. 22.5+/-9.5 ppb) were similar in Bolivians and Caucasians. There was no relationship between pulmonary-artery pressure and respiratory NO in the two groups. These findings provide no evidence that Bolivian high altitude natives are better protected from hypoxic pulmonary hypertension than Caucasian low altitude natives and suggest that attenuation of pulmonary hypertension by increased respiratory NO synthesis may not represent a universal adaptation pattern in highaltitude populations.
Sleep-Disordered Breathing and Vascular Function in Patients With Chronic Mountain Sickness and Healthy High-Altitude Dwellers
(Elsevier BV, 2015) Emrush Rexhaj; Stefano F. Rimoldi; Lorenza Pratali; Roman Brenner; Daniela Andries; Rodrigo Soria; Carlos E. Salinas; Mercedes Villena; Catherine Romero; Yves Allemann
The highs and lows of programmed cardiovascular disease by developmental hypoxia: studies in the chicken embryo
(Wiley, 2017) Nozomi Itani; Carlos E. Salinas; Mercedes Villena; Katie L. Skeffington; Chritian Beck; Eduardo Villamor; C. E. Blanco; Dino A. Giussani
It is now established that adverse conditions during pregnancy can trigger a fetal origin of cardiovascular dysfunction and/or increase the risk of heart disease in later life. Suboptimal environmental conditions during early life that may promote the development of cardiovascular dysfunction in the offspring include alterations in fetal oxygenation and nutrition as well as fetal exposure to stress hormones, such as glucocorticoids. There has been growing interest in identifying the partial contributions of each of these stressors to programming of cardiovascular dysfunction. However, in humans and in many animal models this is difficult, as the challenges cannot be disentangled. By using the chicken embryo as an animal model, science has been able to circumvent a number of problems. In contrast to mammals, in the chicken embryo the effects on the developing cardiovascular system of changes in oxygenation, nutrition or stress hormones can be isolated and determined directly, independent of changes in the maternal or placental physiology. In this review, we summarise studies that have exploited the chicken embryo model to determine the effects on prenatal growth, cardiovascular development and pituitary-adrenal function of isolated chronic developmental hypoxia.
The role of oxygen in prenatal growth: studies in the chick embryo
(Wiley, 2007) Dino A. Giussani; Carlos E. Salinas; Mercedes Villena; Carlos E. Blanco
The compelling evidence linking small size at birth with later cardiovascular disease has renewed and amplified scientific and clinical interests into the determinants of fetal growth. It is accepted that genes and nutrition control fetal growth; however, prior to this study, it had been impossible to isolate the effect of increases and decreases in fetal oxygenation on the regulation of prenatal growth. We investigated the role of oxygen in the control of fetal growth in the chicken because in contrast to mammals, the effects on the fetus of changes in oxygenation could be isolated, by assessing them directly without alteration to the maternal or placental physiology or maternal nutrition during development. The data show that incubation at high altitude of fertilized eggs laid by sea level hens markedly restricted fetal growth. Incubation at high altitude of fertilized eggs laid by high altitude hens also restricted fetal growth, but to a lesser extent compared to eggs laid by sea level hens. By contrast, incubation at sea level of fertilized eggs laid by high altitude hens not only restored, but enhanced, fetal growth relative to sea level controls. Incubation at high altitude of sea level eggs with oxygen supplementation completely prevented the high altitude-induced fetal growth restriction. Thus, fetal oxygenation, independent of maternal nutrition during development, has a predominant role in the control of fetal growth. Further, prolonged high altitude residence confers protection against the deleterious effects of hypoxia on fetal growth.