| Objective:Neurogenic Pulmonary Edema is the acute pulmonary edema by brain injury or central nervous system other diseases without primary heart, lung, kidney and other diseases of the cases. Neurogenic Pulmonary Edema in the pathogenesis has still not very clear, the current doctrine of comparing the two recognized doctrine of blood flow dynamics and pulmonary capillary permeability theory. Hand-foot-mouth disease is the most common cause of NPE that caused by central nervous system infections in children, which clinical features of acute onset, the disease risks of rapid progress, if not cure, patients can be life-threatening. In the treatment program, methylprednisolone is one of the commonly used drug, can reduce capillary permeability and pulmonary edema, but also effectively prevent cerebral edema and block the vicious circle of pulmonary edema-Brain edema. AQP1 was mainly expressed in the lung capillary endothelial cells and alveolar type II cells which play an important role in water transport between alveolar capillaries. In the recent years, studies have shown that the AQP1 expression and activity decreased in acute lung injury, suggesting that AQP1 may be involved in the formation of pulmonary edema; and glucocorticoids such as dexamethasone can upregulate the expression of AQP1 in lung tissue, And on whether methylprednisolone can increase the expression of AQP1 to reduce in the treatment of NPE is rarely reported.In this study, intraperitoneal injection of epinephrine excessive manufacturing model of NPE, with different doses of methylprednisolone intervene, to explore the mechanism of methylprednisolone in the treatment of NPE in rats by studying changes of expression AQP1 and influence of methylprednisolone on them. Methods:1 Animals and groups 10 Wister rats were selected randomly from 60 experimental rats as a normal control group. The rest 50 Wister rats were injected abdominally to induce NPE models by excessive adrena.40 Wister rats were selected randomly divided randomly completely into five groups: model, a, b, and c.2 attern The normal group were injected abdominally by isotonic Na chloride. NPE model group were injected intraperitoneally adrena (1/1000) at 2.7mg/kg about 0.27ml, after 5 min the majority of rats were respiratory rate to speed up, arched back, breathing difficulties can be seen at 20 min and then gradually slows down until it stops breathing becomes shallow, those who showed significantly performance and survived longer than 20min into the NPE group. a, b and c were injected intraperitoneally immediately after dilution methylprednisolone (respectively,10mg/kg,20mg/kg,30mg/kg).3 Lung morphology and AQP1 immunohistochemistry After rats were anesthetized, opened the rats chests and ligation of the trachea, remove the left lungs into 4% paraformaldehyde solution,4℃storage sink to the bottom of the bottle. Gradient dehydrated, embedded in paraffin, sliced, the lung tissue staining and immunohistochemistry.4 Lung wet-to-dry weight ratio Right lungs were measured wet weights on an electronical scale to obtain the wet weight, and then dried in oven at 60℃for 72 h recording the dry weight, calculated W/D.Results:1 W/D in different group of rats In contrast to normal control group(4.59±0.36),W/D in NPE model group(6.50±0.53) were higher obviously(P<0.05); after treatment of MP,W/D in the a, b and c decreased than that in NPE model group(P<0.05). Compared three groups, the c (5.03±0.36) decreased the most, was statistically significant P<0.05).2 Pathological examination In NPE model group, we can seen alveolar structural damage, widened alveolar wall, alveolar capillaries between the diffuse hyperemia, hemorrhage, alveolar space filled with a lot of exudate under light microscope. The lung histopathological displays markedly improved in methylprednisolone treatment group. In normal control group alveolus structure is clear without effusion. Compared NPE group (3.80±0.422) and the a, b, c, the NPE group the highest pathological score; Compared three groups, the c group scores (1.20±0.422) the lowest, statistically(P<0.05).3 AQP1 expression in different group of rats AQP1 express predominantly in microvascular endothelia and to a lesser extent in typeⅡalveolar epithelia cells, AQP1 expression in NPE model group decreased dramatically paralleled with normal control group(P<0.05), methylprednisolone in the treatment groups than in the NPE group AQP1 expression was significantly enhance (P<0.05). To compared a, b and c, the c group the highest density was statistically significant (P<0.05).Conclusions:1 methylprednisolone reduce the W/D weight ratio and relieve the lung injury. Methylprednisolone can treat NPE effectively.2 AQP1 expression in NPE model group decreased dramatically compared with normal control group, so we speculate the expression reduction of AQP1 drop the ability of edema fluid reabsorbtion which probably means one of reasons of pulmonary edema in NPE. After treatment of Methylprednisolone. AQP1 expression increase significantly than that in NPE model group, which shows Methylprednisolone may has beneficial effects on NPE by regulating AQP1 expression in the lungs of rats.3 After injected intraperitoneally methylprednisolone, to compared with the a, b and c, the c group of the highest density of AQP1, there was significant difference shows that AQP1 expression is increased with the increasing doses of methylprednisolone that caused to increased edema fluid reabsorption across the cell membrane capacity to reduce pulmonary edema.
|
PDF Full Text Request