Pulmonary hemorrhage of the newborn is one of severe disorder in varied neonatal diseases, usely is an emergent appearance. Hypoxia,infection and hypothermia are the main reasons of causing pulmonary hemorrhage. But the mechanism of pulmonary hemorrhage of the newborn has not yet been identifed. Mortality rate remains high. Investigation in pathogenesis in NPH has not yet been developed in detail. Minority literatures were reported in domestic , but they were not thorough enough.Researches have confirmed, after hypothermia hypoxia , rewarming and ventilation could caused pulmonary hemorrhage in newborn rats;Main pathology changes in pulmonary hemorrhage were that pulmonary vascular permeability was increased and pulmonary capillary endothelial cells were damaged; Damage in pulmonary vascular endothelial cells were related to oxygen free radical which incresed in pulmonary hemorrhage maybe the result of synthesis and paraseere-tion of ET - 1 in lung tissue.To establish pulmonary hemorrhage model of the newborn rat by dripping exogeneous serotonin (5 - HT) through tracheal intubation, to reflect pathological changes in mankind, to confirm exogeneous serotonin can cause abnormally excretion of endogenous ET - 1 which may induce pulmonary hemorrhage; To study the level MDA in the lung tissue, and the expression of ET - 1 and eNOS in the lung vascular endothelial cell of pulmonary' hemorrhage induced by exogeneous 5 - HT in newborn rat.Through the research, to establish the pulmonary hemorrhage model induced by exogeneous serotonin(5 - HT) in newborn rats,in biochemical level to study the level of MDA in the lung tissue and the expression of ET - land eNOS in thelung vascular endothelial cell of pulmonary hemorrhage induced by exogeneous 5 - HT in newborn rats. To confirm several supposes of the mechanism in pulmonary hemorrhage of the newborn. To provide the experimental evidences for further identifing the pathogenesis and the clinical therapy in pulmonary hemorrhage of newborn.MethodsTo make an animal model of pulmonary hemorrhage: Fifty newborn Wistar rats (age 4 ~5d) were randomly divided into saline control group (group A) and three experimental groups with different concentration of 5 - HT (group B ^ CD). Injecting different concentration of 5 - HT by tracheal intubation into their lungs,then put the rats to death after 4 hours,and observe the morphological changes in the lung of different groups: grade I normal lung, H pulmonary edema, ffi spotted pulmonary hemorrhage, IV focal pulmonary hemorrhage, V diffuse pulmonary hemorrhage, then choose the best concentration of exogeneous 5-HT.Twenty newborn Wistar rats were randomly divided into saline control group (lOrats) and the group with the best concentration of 5 - HT( 10 rats) ; to assay and compare the level of MDA of lung tissue homogenate in PH with different severities.Fifty newborn Wistar rats were randomly divided into saline control group (10 rats) and the group with the best concentration of 5 - HT(40 rats) ;to assay and compare the expression of ET - 1 eNOS in the lung vascular endothelial cell of pulmonary hemorrhage by the method of immunohistochemistry.ResultsDripping different concentrations of 5 - HT from tracheal intubation into lungs can cause different pulmonary hemorrhage. With the increase of concentration of 5 -HT, the severity of pulmonary hemorrhage in group BAgroup C and group D has been shown no different(P > 0. 05) , but in group D, the motality rate of rats was 30% , the rats in group A ^group B and group C were not founed died; The lung volumes of death rats were increased with wine colour and diffusepulmonary hemorrhage.The comparison of MDA concentration in lung tissue; the concentration of MDA in 1 x 10~5mol/ml experimental group was higher than that in saline control group.The comparison of ET - 1 and eNOS in the lung vascular endothelial cell by immunohistochemistry technology; ET - 1 positive expressions were weak in control group, however in groups of pulmonary hemorrhage enhanced remarkably ( P <0. 05)... |