Browsing by Author "Carvajal, Cristobal"
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Item A REDCap application that links researchers, animal facility staff and members of the IACUC in animal health monitoring(Sage Journals, 2019) Carvajal, Cristobal; Vallejos, Catalina; Lemaitre, Dominique; Ruiz, Jorge; Guzmán, Camila; Aguilera, Valentina; Baño, Diego; Calligaris, SebastiánLos estudios de investigación que requieren la experimentación con animales son regulados por el Comité Institucional para el Cuidado y Uso de Animales de Laboratorio (CICUAL). Con este fin, el CICUAL debe integrar la información suministrada por los investigadores de cada estudio preclínico y por los veterinarios de Bioterio para poder controlar y aprobar el proceso. Utilizar un sistema en papel para recoger datos del bienestar y la salud de los animales es una práctica común pero que requiere mucho tiempo, propensa a errores de lectura y transcripción, sin nombrar todos los inconvenientes que tiene para veterinarios e investigadores que desean tomar decisiones colaborativas y precisas cuando el bienestar del animal está en peligro. Hemos creado un Sistema Web para gestión de bases de datos que se centra en la salud animal con el potencial de mejorar su bienestar. El sistema de gestión de datos utiliza el software REDCap, que permite la integración de datos para ofrecer una solución para la evaluación del bienestar animal. El programa propuesto incluye indicadores claves del estado de salud general, como el entorno, información física/nutricional y parámetros de comportamiento durante la cría y la experimentación con animales, como componentes importantes del bienestar animal. Asimismo, el sistema facilita la comunicación de esta información entre los investigadores, el personal de Bioterio y el CICUAL. REDCap está disponible para organizaciones sin fines de lucro de lucro y adáptandose a los requerimientos propios de las instituciones interesadas y responsables del cuidado de animales utilizados en los estudios de investigación. REDCap es una herramienta excelente para fomentar buenas prácticas que beneficien la salud de los animales de experimentación.Item Angiotensin-converting enzyme insertion/deletion polymorphism is associated with severe hypoxemia in pediatric ARDS(Springer, 2012) Cruces, Pablo; Puga, Alonso; Erranz, Benjamín; Donoso, Alejandro; Carvajal, Cristobal; Wilhelm, Jan; Repetto, GabrielaPURPOSE: The D allele of the insertion/deletion (I/D) polymorphism of a 287-bp sequence in the angiotensin-converting enzyme (ACE) gene has been associated with an increased activity of this enzyme. Its role in susceptibility to acute respiratory distress syndrome (ARDS) has not been well defined. We hypothesized that ACE I/D genotype in pediatrics is associated with ARDS and plasma levels of angiotensin II. METHODS: Prospective case-control study in patients under 15 years of age from a mixed Chilean population. Sixty patients with ARDS and 60 controls were included. Association between ACE genotype and ARDS was evaluated as the primary outcome; mortality and severe hypoxemia were examined as secondary outcomes. Plasma angiotensin-II concentration was measured by immunoassay at admission. RESULTS: Frequency of ACE I/D genotype was similar in ARDS and control groups (p = 0.18). In the ARDS group, severe hypoxemia was less frequent in D allele carriers (p < 0.05). Plasma angiotensin-II levels were associated with genotype in the ARDS group, but not controls, being higher in D allele carriers (p = 0.016). CONCLUSION: These data do not support the association between ACE I/D genotype and ARDS, although severe hypoxemia was less frequent in D allele carriers. ACE I/D polymorphism modified angiotensin-II levels in pediatric ARDS, but its pathogenic role is not well understood and needs to be addressed in future studies.Publication Characteristics of Medically Transported Critically Ill Children with Respiratory Failure in Latin America: Implications for Outcomes(2021) Serra, Jesus; Díaz, Franco; Cruces, Pablo; Carvajal, Cristobal; Nuñez, Maria; Donoso, A.; Bravo, J A; Carbonell, M.; Courtie, C.; Fernández. A.; Martínez, L.; Martínez, J.; Menta, S.; Pedrozo, Luis; Wegner, A.; Monteverde, Nicolas; Jaramillo, Juan; Jabornisky, Roberto; González, Sebastián; Kudchadkar, Sapna; Vásquez, Pablo; On behalf of LARed NetworkSeveral challenges exist for referral and transport of critically ill children in resource-limited regions such as Latin America; however, little is known about factors associated with clinical outcomes. Thus, we aimed to describe the characteristics of critically ill children in Latin America transferred to pediatric intensive care units for acute respiratory failure to identify risk factors for mortality. We analyzed data from 2,692 patients admitted to 28 centers in the Pediatric Collaborative Network of Latin America Acute Respiratory Failure Registry. Among patients referred from another facility (773, 28%), nonurban transports were independently associated with mortality (adjusted odds ratio = 9.4; 95% confidence interval: 2.4-36.3).Item Mild hypothermia increases pulmonary anti-inflammatory response during protective mechanical ventilation in a piglet model of acute lung injury(John Wiley & Sons, 2013) Cruces, Pablo; Erranz, Benjamín; Donoso, Donoso; Carvajal, Cristobal; Salomon, Tatiana; Torres, Maria; Diaz, FrancoBACKGROUND: The effects of mild hypothermia (HT) on acute lung injury (ALI) are unknown in species with metabolic rate similar to that of humans, receiving protective mechanical ventilation (MV). We hypothesized that mild hypothermia would attenuate pulmonary and systemic inflammatory responses in piglets with ALI managed with a protective MV. METHODS: Acute lung injury (ALI) was induced with surfactant deactivation in 38 piglets. The animals were then ventilated with low tidal volume, moderate positive end-expiratory pressure (PEEP), and permissive hypercapnia throughout the experiment. Subjects were randomized to HT (33.5°C) or normothermia (37°C) groups over 4 h. Plasma and tissue cytokines, tissue apoptosis, lung mechanics, pulmonary vascular permeability, hemodynamic, and coagulation were evaluated. RESULTS: Lung interleukin-10 concentrations were higher in subjects that underwent HT after ALI induction than in those that maintained normothermia. No difference was found in other systemic and tissue cytokines. HT did not induce lung or kidney tissue apoptosis or influence lung mechanics or markers of pulmonary vascular permeability. Heart rate, cardiac output, oxygen uptake, and delivery were significantly lower in subjects that underwent HT, but no difference in arterial lactate, central venous oxygen saturation, and coagulation test was observed. CONCLUSIONS: Mild hypothermia induced a local anti-inflammatory response in the lungs, without affecting lung function or coagulation, in this piglet model of ALI. The HT group had lower cardiac output without signs of global dysoxia, suggesting an adaptation to the decrease in oxygen uptake and delivery. Studies are needed to determine the therapeutic role of HT in ALI.Item Surfactant deactivation in a pediatric model induces hypovolemia and fluid shift to the extravascular lung compartment(John Wiley & Sons, 2013) Diaz, Franco; Erranz, Benjamín; Donoso, Alejandro; Carvajal, Cristobal; Salomon, Tatiana; Torres, Maria; Cruces, PabloBACKGROUND: Surfactant deficiency is the pivotal abnormality in Neonatal and Acute Respiratory Distress Syndrome. Surfactant deactivation can produce hypoxemia, loss of lung compliance, and pulmonary edema, but its circulatory consequences are less understood. OBJECTIVE: To describe the sequential hemodynamic changes and pulmonary edema formation after surfactant deactivation in piglets. METHODS: Surfactant deactivation was induced by tracheal instillation of polysorbate 20 in 15 anesthetized and mechanically ventilated Large White piglets. The hemodynamic consequences of surfactant deactivation were assessed at 30, 120, and 240 min by transpulmonary thermodilution and traditional methods. RESULTS: Surfactant deactivation caused hypoxemia, reduced lung compliance, and progressively increased lung water content (P < 0.01). Early hypovolemia was observed, with reductions of the global end-diastolic volume and stroke volume (P < 0.05). Reduced cardiac output was observed at the end of the study (P < 0.05). Standard monitoring was unable to detect these early preload alterations. Surprisingly, the bronchoalveolar protein content was greatly increased at the end of the study compared with baseline levels (P < 0.01). This finding was inconsistent with the notion that the pulmonary edema induced by surfactant deactivation was exclusively caused by high surface tension. CONCLUSIONS: Hypovolemia develops early after surfactant deactivation, in part due to the resulting fluid shift from the intravascular compartment to the lungs.