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Andes virus (ANDV), a member of the Orthohantavirus genus in the Hantaviridae family, has a trisegmented, single-stranded RNA-genome and is the etiologic agent of hantavirus cardiopulmonary syndrome (HCPS) in Chile [...]

An estimated human population of 170 million inhabit at high-altitude (HA, above 2,500 m). The potential pathological effects of HA hypobaric hypoxia during gestation have been the focus of several researchers around the world. The studies based on the Himalayan and Central/South American mountains are particularly interesting as these areas account for nearly 70% of the HA world population. At present, studies in human and animal models revealed important alterations in fetal development and growth at HA. Moreover, vascular responses to chronic hypobaria in the pregnant mother and her fetus may induce marked cardiovascular impairments during pregnancy or in the neonatal period. In addition, recent studies have shown potential long-lasting postnatal effects that may increase cardiovascular risk in individuals gestated under chronic hypobaria. Hence, the maternal and fetal adaptive responses to hypoxia, influenced by HA ancestry, are vital for a better developmental and cardiovascular outcome of the offspring. This mini-review exposes and discusses the main determinants of vascular dysfunction due to developmental hypoxia at HA, such as the Andean Mountains, at the maternal and fetal/neonatal levels. Although significant advances have been made from Latin American studies, this area still needs further investigations to reveal the mechanisms involved in vascular dysfunction, to estimate complications of pregnancy and postnatal life adequately, and most importantly, to determine potential treatments to prevent or treat the pathological effects of being developed under chronic hypobaric hypoxia.

In this study, we assessed the effects of Atrial Natriuretic Peptide (ANP) and Cinaciguat, as experimental medicines to treat neonatal lambs exposed to chronic hypoxic conditions. To compare the different treatments, the mechanical responses of aorta, carotid, and femoral arterial walls were analyzed by means of axial pre-stretch and ring-opening tests, through a study with n = 6 animals for each group analyzed. The axial pre-stretch test measures the level of shortening in different zones of the arteries when extracted from lambs, while the ring-opening test is used to quantify the degree of residual circumferential deformation in a given zone of an artery. In addition, histological studies were carried out to measure elastin, collagen, and smooth muscle cell (SMC) nuclei densities, both in control and treated groups. The results show that mechanical response is related with histological results, specifically in the proximal abdominal aorta (PAA) and distal carotid zones (DCA), where the cell nuclei content is related to a decrease of residual deformations. The opening angle and the elastic fibers of the aorta artery were statistically correlated (p < 0.05). Specifically, in PAA zone, there are significant differences of opening angle and cell nuclei density values between control and treated groups (p-values to opening angle: Control-ANP = 2 ⋅ 10–2, Control-Cinaciguat = 1 ⋅ 10–2; p-values to cell nuclei density: Control-ANP = 5 ⋅ 10–4, Control-Cinaciguat = 2 ⋅ 10–2). Respect to distal carotid zone (DCA), significant differences between Control and Cinaciguat groups were observed to opening angle (p-value = 4 ⋅ 10–2), and cell nuclei density (p-value = 1 ⋅ 10–2). Our findings add evidence that medical treatments may have effects on the mechanical responses of arterial walls and should be taken into account when evaluating the complete medical outcome.

Neonatal lambs, as other neonates, have physiologically a very low plasma melatonin concentration throughout 24 h. Previously, we found that melatonin given to neonates daily for 5 days decreased heart weight and changed plasma cortisol and gene expression in the adrenal and heart. Whether these changes could compromise the responses to life challenges is unknown. Therefore, firstly, we studied acute effects of melatonin on the defense mechanisms to acute hypoxia in the neonate. Eleven lambs, 2 weeks old, were instrumented and subjected to an episode of acute isocapnic hypoxia, consisting of four 30 min periods: normoxia (room air), normoxia after an i.v. bolus of melatonin (0.27 mg kg−1, n = 6) or vehicle (ethanol 1:10 NaCl 0.9%, n = 5), hypoxia (PaO2: 30 ± 2 mmHg), and recovery (room air). Mean pulmonary and systemic blood pressures, heart rate, and cardiac output were measured, and systemic and pulmonary vascular resistance and stroke volume were calculated. Blood samples were taken every 30 min to measure plasma norepinephrine, cortisol, glucose, triglycerides, and redox markers (8-isoprostane and FRAP). Melatonin blunted the increase of pulmonary vascular resistance triggered by hypoxia, markedly exacerbated the heart rate response, decreased heart stroke volume, and lessened the magnitude of the increase of plasmatic norepinephrine and cortisol levels induced by hypoxia. No changes were observed in pulmonary blood pressure, systemic blood pressures and resistance, cardiac output, glucose, triglyceride plasma concentrations, or redox markers. Melatonin had no effect on cardiovascular, endocrine, or metabolic variables, under normoxia. Secondly, we examined whether acute melatonin administration under normoxia could have an effect in gene expression on the adrenal, lung, and heart. Lambs received a bolus of vehicle or melatonin and were euthanized 30 min later to collect tissues. We found that melatonin affected expression of the immediate early genes egr1 in adrenal, ctgf in lung, and nr3c1, the glucocorticoid receptor, in adrenal and heart. We speculate that these early gene responses may contribute to the observed alterations of the newborn defense mechanisms to hypoxia. This could be particularly important since the use of melatonin is proposed for several diseases in the neonatal period in humans.

The article discusses the discovery of ticks parasitizing Rhinella horribilis in Mexico, specifically Amblyomma rotundatum in the state of Nuevo Leon, and describes the death feigning behavior observed in Rhinella atacamensis in Chile.

Pulmonary arterial hypertension of the neonate (PAHN) is a pathophysiological condition characterized by maladaptive pulmonary vascular remodeling and abnormal contractile reactivity. This is a multifactorial syndrome with chronic hypoxia and oxidative stress as main etiological drivers, and with limited effectiveness in therapeutic approaches. Melatonin is a neurohormone with antioxidant and vasodilator properties at the pulmonary level. Therefore, this study aims to test whether a postnatal treatment with melatonin during the neonatal period improves in a long‐lasting manner the clinical condition of PAHN. Ten newborn lambs gestated and born at 3600 m were used in this study, five received vehicle and five received melatonin in daily doses of 1 mg kg−1 for the first 3 weeks of life. After 1 week of treatment completion, lung tissue and small pulmonary arteries (SPA) were collected for wire myography, molecular biology, and morphostructural analyses. Melatonin decreased pulmonary arterial pressure the first 4 days of treatment. At 1 month old, melatonin decreased the contractile response to the vasoconstrictors K+, TX2, and ET‐1. Further, melatonin increased the endothelium‐dependent and muscle‐dependent vasodilation of SPA. Finally, the treatment decreased pulmonary oxidative stress by inducing antioxidant enzymes and diminishing pro‐oxidant sources. In conclusion, melatonin improved vascular reactivity and oxidative stress at the pulmonary level in PAHN lambs gestated and born in chronic hypoxia. [ABSTRACT FROM AUTHOR]