RESUMO
Neonatal asphyxia occurs due to reduction in oxygen supply to vital organs in the newborn. Rapid restoration of oxygen to the lungs after a long period of asphyxia can cause lung injury and decline of respiratory function, which result from the activity of molecules that induce vascular changes in the lung such as nitric oxide (NO) and vascular endothelial growth factors (VEGF). In this study, we evaluated the pulmonary and vascular morphometry of rats submitted to the model of neonatal asphyxia and mechanical ventilation, their expression of pulmonary VEGF, VEGF receptors (VEGFR-1/VEGFR-2), and endothelial NO synthase (eNOS). Neonate Sprague-Dawley rats (CEUA #043/2011) were divided into four groups (n=8 each): control (C), control submitted to ventilation (CV), hypoxia (H), and hypoxia submitted to ventilation (HV). The fetuses were harvested at 21.5 days of gestation. The morphometric variables measured were body weight (BW), total lung weight (TLW), left lung weight (LLW), and TLW/BW ratio. Pulmonary vascular measurements, VEGFR-1, VEGFR-2, VEGF, and eNOS immunohistochemistry were performed. The morphometric analysis showed decreased TLW and TLW/BW ratio in HV compared to C and H (P<0.005). Immunohistochemistry showed increased VEGFR-2/VEGF and decreased VEGFR-1 expression in H (P<0.05) and lower eNOS expression in H and HV. Median wall thickness was increased in H, and the expression of VEGFR-1, VEGFR-2, VEGF, and eNOS was altered, especially in neonates undergoing H and HV. These data suggested the occurrence of arteriolar wall changes mediated by NO and VEGF signaling in neonatal hypoxia.
Assuntos
Asfixia Neonatal/terapia , Pulmão/patologia , Óxido Nítrico Sintase Tipo III/análise , Respiração Artificial/efeitos adversos , Fator A de Crescimento do Endotélio Vascular/análise , Receptor 1 de Fatores de Crescimento do Endotélio Vascular/análise , Receptor 2 de Fatores de Crescimento do Endotélio Vascular/análise , Animais , Arteríolas/patologia , Asfixia Neonatal/patologia , Asfixia Neonatal/fisiopatologia , Modelos Animais de Doenças , Imuno-Histoquímica , Pulmão/irrigação sanguínea , Pulmão/fisiopatologia , Ratos Sprague-Dawley , Valores de Referência , Respiração Artificial/métodosRESUMO
Neonatal asphyxia occurs due to reduction in oxygen supply to vital organs in the newborn. Rapid restoration of oxygen to the lungs after a long period of asphyxia can cause lung injury and decline of respiratory function, which result from the activity of molecules that induce vascular changes in the lung such as nitric oxide (NO) and vascular endothelial growth factors (VEGF). In this study, we evaluated the pulmonary and vascular morphometry of rats submitted to the model of neonatal asphyxia and mechanical ventilation, their expression of pulmonary VEGF, VEGF receptors (VEGFR-1/VEGFR-2), and endothelial NO synthase (eNOS). Neonate Sprague-Dawley rats (CEUA #043/2011) were divided into four groups (n=8 each): control (C), control submitted to ventilation (CV), hypoxia (H), and hypoxia submitted to ventilation (HV). The fetuses were harvested at 21.5 days of gestation. The morphometric variables measured were body weight (BW), total lung weight (TLW), left lung weight (LLW), and TLW/BW ratio. Pulmonary vascular measurements, VEGFR-1, VEGFR-2, VEGF, and eNOS immunohistochemistry were performed. The morphometric analysis showed decreased TLW and TLW/BW ratio in HV compared to C and H (P<0.005). Immunohistochemistry showed increased VEGFR-2/VEGF and decreased VEGFR-1 expression in H (P<0.05) and lower eNOS expression in H and HV. Median wall thickness was increased in H, and the expression of VEGFR-1, VEGFR-2, VEGF, and eNOS was altered, especially in neonates undergoing H and HV. These data suggested the occurrence of arteriolar wall changes mediated by NO and VEGF signaling in neonatal hypoxia.
Assuntos
Animais , Asfixia Neonatal/terapia , Respiração Artificial/efeitos adversos , Receptor 1 de Fatores de Crescimento do Endotélio Vascular/análise , Receptor 2 de Fatores de Crescimento do Endotélio Vascular/análise , Fator A de Crescimento do Endotélio Vascular/análise , Óxido Nítrico Sintase Tipo III/análise , Pulmão/patologia , Arteríolas/patologia , Valores de Referência , Asfixia Neonatal/fisiopatologia , Asfixia Neonatal/patologia , Respiração Artificial/métodos , Imuno-Histoquímica , Ratos Sprague-Dawley , Modelos Animais de Doenças , Pulmão/fisiopatologia , Pulmão/irrigação sanguíneaRESUMO
Relatam-se um caso de cisto hidatico retrovesical isolado em um homem de 36 anos, com queixas de acentuada dificuldade miccional e mostrando, ao exame fisico, massa globosa e tensa na regiao suprapubica, que persistiu apos cateterizacao vesical. A cistografia revelou sinais de massa retrovesical, determinando compressao extrinseca na bexiga. O diagnostico foi confirmado durante a exploracao cirurgica. Nao foi descoberta doenca hidatica em nenhuma outra localizacao (e.g.: figado, pulmao, etc.). Discute-se tambem a provavel via de instalacao do cisto nessa situacao rara
Assuntos
Adulto , Humanos , Masculino , Doenças da Bexiga Urinária , EquinococoseRESUMO
Os autores relatam um caso de pseudo tumor renal determinado por hipertrofia nodular compensatoria em virtude de trombose da arteria renal. A hipotese de lesao expansiva solida foi sugerida tanto pela ultrasonografia como pela nefrotomografia. Na internacao o paciente apresentava quadro de hipertensao arterial severa, e poliglobulia importante. Manifestacoes estas que desapareceram apos a nefrectomia