Características de neonatos com síndrome do desconforto respiratório considerando a via de parto em uma unidade de terapia intensiva da região central do RS / Characteristics of neonates with respiratory distress syndrome admitted to an intensive care unit of the central region of RS

Objetivo: Analisar as características dos neonatos com Síndro-me do Desconforto Respiratório (SDR), considerando a via de parto, admitidos em uma Unidade de Terapia Intensiva de um hospital universitário da região central do Rio Grande do Sul. Materiais e métodos: Estudo retrospectivo, realizado no período de abril a maio de 2017, através da análise de prontuários de neonatos com idade gestacional acima de 37 semanas, ambos os sexos, internados no ano de 2016 na Unidade de Terapia Intensiva Neonatal (UTIN) do Hospital Universitário de Santa Maria com CID 10 P22 ­ Desconforto (angústia) respiratório(a) do recém-nascido. Resultados: A amostra foi constituída por 40 registros de nascimentos (25 do sexo masculino), divididos em parto vaginal (n=11) e cesárea (n=29), representando 27,5% e 72,5%, respectivamente, das internações totais. A média de idade materna foi de 27±7 anos, com uma média de 7±5 con-sultas pré-natais. Durante o período de internação 65%(n=26) dos 40 neonatos necessitaram de oxigenoterapia. Conclusão:A partir dos resultados obtidos no presente estudo, observamos que a SDR representa 11% das internações ocorridas na UTIN, no ano de 2016. A prevalência, quanto ao tipo de parto, foi de neonatos nascidos de cesariana, sem a presença do trabalho de parto e com idade gestacional de 38 semanas. (AU)

Objective: To analyze the characteristics of newborns with Respiratory Distress Syndrome (RDS), considering the route of delivery, admitted to an Intensive Care Unit of a university hospital in the central region of Rio Grande do Sul, Brazil. Materials and methods: A retrospective study, conducted from April to May 2017, through the analysis of records of neonates with gestational age above 37 weeks, both sexes, hospitalized in 2016 at the Neonatal Intensive Care Unit (NICU) of the Uni-versity Hospital of Santa Maria, with ICD 10 P22 - Respiratory distress syndrome of newborn. Results: The sample consisted of 40 birth records (25 males), divided into vaginal (n = 11) and caesarean (n = 29), representing 27.5% and 72.5%, respective-ly, of total hospitalization. The mean maternal age was 27 ± 7 years, with a mean of 7 ± 5 prenatal consultations. During the hospitalization period, 65% (n = 26) of the 40 neonates required oxygen therapy. Conclusion: Based on the results obtained in the present study, we observed that the RDS represents 11% of the hospitalizations that occurred in the NICU in 2016. The prevalence, in terms of route delivery, was of neonates born caesarean, without the presence of labor and gestational age of 38 weeks. (AU)

Ulinastatin attenuates lipopolysaccharide-induced acute lung injury by intervening p38 MAPK/ERK signaling pathway / 中国药理学通报

Aim To investigate whether ulinastatin has a beneficial effect on lipopolysaccharide( LPS) induced acute respiratory distress syndrome ( ARDS ) in rats, and to explore the possible underlying mechanisms. Methods Fifty-six Wistar rats were randomly as-signed into control group, model group( LPS 6,12,24 h groups), ulinastatin group(UTI 6,12,24 h groups), with 8 in each group. ARDS rat model was reproduced by intraperitoneal injection of LPS ( 10 mg · kg-1 ) , The rats in UTI groups were injected ulinastatin (20 000 u·kg-1), The rats in the control group re-ceived an equal volume of normal saline at the same time, rats in each group were sacrificed at 6,12,24 hours after LPS challenge. Plasma and lung tissue sam-ples were collected, Histopathological evaluation, lung wet/dry (W/D) ratio, Tumor necrosis factor-a(TNF-α) , Interleukin-18 ( IL-18 ) , surfactant protein A ( SPA) , malondialdehyde ( MDA ) , nitric oxide ( NO ) and superoxide dismutase( SOD) were analyzed. Immu-nohistochemical method was performed to detect the protein expression of p38MAPK and ERK. Western blot method was used to detect lung phosphorylated p38 MAPK ( p-p38 MAPK ) and pERK protein expres-sion changes. Result In the control groups, lung tis-sue showed a normal structure and clear pulmonary al-veoli under a light microscope. In the model group, ARDS characters such as extensive thickening of the alveolar wall, significant infiltration of inflammatory cells, demolished structure of pulmonary alveoli, and hemorrhage were found. In the all UTI treatment groups, these pathological changes in lung were markedly alleviated compared with those of LPS-in-duced ARDS group. Compared with control groups, lung W/D ratio, tumor necrosis factor-a ( TNF-α) , in-terleukin-18 ( IL-18 ) and surfactant protein A ( SPA ) in plasma ,and lung MDA,NO levels in lung homogenates in the LPS group were increased significantly, while the lung SOD levels in the LPS group were decreased. Compared with the LPS group, lung W/D ratio, TNF-aIL-18 and ( SPAin plasma , and lung MDA levels in lung homogenates in the UTI groups were decreased significantly, while the lung SOD levels in the UTI groups were increased. Immunohistochemistry showed that positive expressions of p38 MAPK and ERK in cy-toplasm and nucleus in the ulinastatin treatment groups were significantly lower than those in the model group. Western blot showed that compared with the control group, the p-p38MAPK and pERK protein expression in LPS group were significantly increased, and the uli-nastatin could inhibit the protein expressions compared with model group. Conclusion Ulinastatin can signifi-cantly ameliorate the lung injury induced by LPS in rats via the intervention of p38 MAPK and ERK signa-ling pathway and reducing inflammation and antioxidant effect.

Role of CREB in LPS-induced injury of RPMVEC / 中国药理学通报

Aim To investigate the role of cAMP re-sponse element binding protein (CREB)in the injury of rat pulmonary microvascular endothelial cell (RPM-VEC)induced by LPS.Methods RPMVECs were i-solated and cultured in vitro,Western-blot was used to assay phosphorylation levels of CREB.Endothelial per-meability was determined by measuring the influx of Evans blue-labeled albumin across endothelial mono-layer.Results LPS increased CREB phosphorylation at Ser 1 3 3 in RPMVEC in a time-dependent manner , peaked at 30 min,but still higher at 120 min compared with basal control group.Pretreatment of cells with PKA inhibitor V5681 nearly suppressed the CREB phosphorylation stimulated in the presence of LPS,and the monolayer permeability of PMVEC was significantly increased. Conclusions LPS rapidly induces the phosphorylation of CREB in RPMVEC,and PKA me-diates the process.During the process of LPS-stimula-ted injury of RPMVEC,phosphorylation of CREB may play a protective role.