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      Transplacental transfer of medetomidine and ketamine in pregnant ewes

      1 , 2 , 2 , 3
      Laboratory Animals
      SAGE Publications

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          Brief, large tidal volume ventilation initiates lung injury and a systemic response in fetal sheep.

          Premature infants are exposed to potentially injurious ventilation in the delivery room. Assessments of lung injury are confounded by effects of subsequent ventilatory support. To evaluate the injury response to a brief period of large tidal volume (Vt) ventilation, simulating neonatal resuscitation in preterm neonates. Preterm lambs (129 d gestation; term is150 d) were ventilated (Vt = 15 ml/kg, no positive end-expiratory pressure) for 15 minutes to simulate delivery room resuscitation, either with the placental circulation intact (fetal resuscitation [ FR]) or after delivery (neonatal resuscitation [NR]). After the initial 15 minutes, lambs received surfactant and were maintained with either ventilatory support (FR-VS and NR-VS) or placental support (FR-PS) for 2 hours, 45 minutes. A control group received no resuscitation and was maintained with placental support. Samples of bronchoalveolar lavage fluid, lung, and liver were analyzed. Inflammatory cells and protein in bronchoalveolar lavage fluid, heat shock protein-70 immunostaining, IL-1beta, IL-6, IL-8, monocyte chemotactic protein-1, serum amyloid A (SAA)-3, Toll-like receptor (TLR)-2, and TLR4 mRNA in the lungs were increased in the FR-PS group compared with control animals. There were further elevations in neutrophils, IL-6, and IL-8 mRNA in the FR-VS and NR-VS groups compared with FR-PS. SAA3, TLR2, and TLR4 mRNA increased in the liver in all resuscitation groups relative to control animals. Ventilation for 15 minutes with a Vt of 15 ml/kg initiates an injurious process in the preterm lung and a hepatic acute-phase response. Subsequent ventilatory support causes further increases in some injury indicators.
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            Airway injury from initiating ventilation in preterm sheep.

            Premature infants exposed to ventilation are at risk of developing bronchopulmonary dysplasia and persistent lung disease in childhood. We report where injury occurred within the lung after brief ventilation at birth. Preterm sheep (129 d gestation) were ventilated with an escalating tidal volume to 15 mL/kg by 15 min to injure the lungs, with the placental circulation intact (fetal) or after delivery (newborn). Fetal lambs were returned to the uterus for 2 h 45 min, whereas newborn lambs were maintained with gentle ventilatory support for the same period. The control group was not ventilated. Bronchoalveolar lavage fluid (BALF) and lung tissue were analyzed. In both fetal and newborn lambs, ventilation caused bronchial epithelial disruption in medium-sized airways. Early growth response protein 1 (Egr-1), monocyte chemotactic protein 1 (MCP-1), IL-6, and IL-1beta mRNA increased in the lung tissue from fetal and newborn lambs. Egr-1, MCP-1, and IL-6 mRNA were induced in mesenchymal cells surrounding small airways, whereas IL-1beta mRNA localized to the epithelium of medium/small airways. Ventilation caused loss of heat shock protein 70 (HSP70) mRNA from the bronchial epithelium, but induced mRNA in the smooth muscle surrounding large airways. HSP70 protein decreased in the lung tissue and increased in BALF with ventilation. Initiation of ventilation induced a stress response and inflammatory cytokines in small and medium-sized airways.
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              Characterization of the selectivity, specificity and potency of medetomidine as an α2-adrenoceptor agonist

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                Author and article information

                Journal
                Laboratory Animals
                Lab Anim
                SAGE Publications
                0023-6772
                1758-1117
                January 2012
                January 2012
                January 2012
                January 2012
                : 46
                : 1
                : 46-50
                Affiliations
                [1 ]School of Veterinary and Biomedical Sciences, Murdoch University, Western Australia 6150, Australia
                [2 ]School of Pharmacy, Murdoch University, Western Australia 6150, Australia
                [3 ]Separation Science and Metabolomics Laboratory, Murdoch University, Western Australia 6150, Australia
                Article
                10.1258/la.2011.010179
                22008849
                ee0c02e3-1903-459f-9e80-4f101cc738fb
                © 2012

                http://journals.sagepub.com/page/policies/text-and-data-mining-license

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