Browsing by Autor "Dino A. Giussani"

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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.
Graduated effects of high-altitude hypoxia and highland ancestry on birth size
(Springer Nature, 2013) Rudy Soria; Colleen G. Julian; Enrique Vargas; Lorna G. Moore; Dino A. Giussani
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.
Parental ancestry and risk of early pregnancy loss at high altitude
(Wiley, 2020) Imogen Grant; Rudy Soria; Colleen G. Julian; Enrique Vargas; Lorna G. Moore; Catherine Aiken; Dino A. Giussani
High altitude pregnancy is associated with increased frequency of low birth weight infants and neonatal complications, the risks of which are higher in women of low-altitude ancestry. Does ancestry also influence the risk of miscarriage (pregnancy loss <20 weeks) in high-altitude pregnancy? To answer this, 5386 women from La Paz, Bolivia (3300-4150 m) with ≥1 live-born infant were identified. Data were extracted from medical records including maternal and paternal ancestry, demographic factors, and reproductive history. The risk of miscarriage by ancestry was assessed using multivariate logistic regression, adjusting for parity, and maternal age. Andean women experienced first live-births younger than Mestizo or European women (21.7 ± 4.6 vs 23.4 ± 8.0 vs 24.1 ± 5.1, P < .001). Andeans experienced more pregnancies per year of reproductive life (P < .001) and had significantly higher ratios of live-births to miscarriages than women of Mestizo or European ancestry (P < .001). Andean women were 24% less likely to have ever experienced a miscarriage compared to European women (OR:0.76; CI:0.62-0.90, P < .001). The woman's partner's ancestry wasn't a significant independent predictor of miscarriage. In conclusion, the risk of miscarriage at high altitude is lower in Andean women. The lack of a paternal ancestry effect suggests underlying mechanisms relate more to differential maternal adaptation in early pregnancy than fetal genetics.
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.