| Pulmonary hemorrhage of the newborn (PHN), a common fatal disease in neonatal intensive care unit (NICU), reaches a high mortality rate of 40%~50%. The most frequently seen predisposing causes of PHN include severe infection, acute pulmonary ischemia and hypoxia in the perinatal period, cold injury or hypothermia, premature birth and low birth weight. The pathogenesis is not clearly known yet, it was proposed that injury by infection-immunocomplex, hemorrhage pulmonary edema due to the left heart failure and impaired function blood coagulation contribute to the PHN, yet all of the above hypotheses fail to be the thoroughly clear mechanism for PHN. In the recent years, researchers have confirmed that the pathogenesis of pulmonary hemorrhage is attributed to the stress failure of the pulmonary capillaries, which are manifested as the injury of the endothelium of pulmonary capillaries and alveolar epithelium, in addition, the ultimate cause of the stress failure is confirmed to be the increase in pressure in the pulmonary artery and capillary. Dr. Han and coworkers have found that most of the children suffering from shock are dead of respiratory failure and pulmonary bleeding. They reported that the diffuse invasive changes is seen on the X-ray film, on the pathological sections the formation of hyaline membrane on some part of the pulmonary alveolar wall is observed in addition to the bleeding phenomenon. Under the electron microscope, the changes arethe destruction of the capillary endothelial cells and type II alveolar endothelial cells. Dr. Li and coworkers have reported in their clinical studies that the pulmonary artery pressure is significantly increased in PHN. All these observations indicate that PHN share similar pathological and blood dynamic changes with acute respiratory distress syndrome (ARDS), i.e. both are manifested as destruction of pulmonary alveolar capillary membrane and high pressure of pulmonary artery. Therefore we predict that PHN, similar to ARDS, is a lung injury syndrome caused by various pathogenic factors in the final stage of certain diseases, is a special form of ARDS in the neonatal period, the pathogenesis of PHN is likely to be relevant with that of ARDS.ARDS is the result of uncontrolled inflammatory responses in the lung due to various causes, is the severe stage of ALI (ALI). Currently it is regarded that the start-up stage of the inflammation involves a complex interaction between inflammatory cells and tissue cells. The initiation starts with the activation of transcription factor nuclear factor kappa B (NF-kB), which regulate the gene transcription of different inflammation promoting factors (e.g. TNF-a , IL-lp etc) and intercellular adhesion molecules (e.g. ICAM-1 etc). Thus PMN are promoted to aggregate, adhere, activate and release a large amount of active oxygen, proteinase and inflammation mediators. The above processes act as a local inflammatory response, but the over-reaction of may lead to the injury in the pulmonary alveolar-capillary membrane, decrease in the pulmonary surfactant (PS) and impaired functions. The clinical manifestation is named ALI/ARDS, its typical pathological feature is the diffuse destruction of the alveolar-capillary membrane. 40% of the Lung tissue is composed of endothelial cells, the injury to these cells may lead to bleeding, blood coagulation in the vessels and disturbed regulation of blood vessel tension, these promote the formation of high pulmonary artery pressure. Pulmonary bleeding is the core basis of pathogenesis in ALI/ARDS. Until present, there has been no report on the relevance between PHN and ALI/ARDS in China and abroad.To confirm our hypothesis, the current study used lipopolysaccharides(LPS) to produce newborn and adult Wistar rat models, studied the effect of LPS on the lung tissue of neonatal rats by morphological, biochemical and molecular biological methods. Our result answered the questions like whether LPS can induce the lung injury in neonatal rats, pulmonary bleeding and investigated the mechanism...
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