ABSTRACT
OBJECTIVE: The objective of this study was to evaluate the involvement of peripheral nitric oxide (NO) in vagotomy-induced pulmonary edema by verifying whether the nitric oxide synthases (NOS), constitutive (cNOS) and inducible (iNOS), participate in this mechanism. INTRODUCTION: It has been proposed that vagotomy induces neurogenic pulmonary edema or intensifies the edema of other etiologies. METHODS: Control and vagotomized rats were pretreated with 0.3 mg/kg, 3.0 mg/kg or 39.0 mg/kg of L-NAME, or with 5.0 mg/kg, 10.0 mg/kg or 20.0 mg/kg of aminoguanidine. All animals were observed for 120 minutes. After the animals' death, the trachea was catheterized in order to observe tracheal fluid and to classify the severity of pulmonary edema. The lungs were removed and weighed to evaluate pulmonary weight gain and edema index. RESULTS: Vagotomy promoted pulmonary edema as edema was significantly higher than in the control. This effect was modified by treatment with L-NAME. The highest dose, 39.0 mg/kg, reduced the edema and prolonged the survival of the animals, while at the lowest dose, 0.3 mg/kg, the edema and reduced survival rates were maintained. Aminoguanidine, regardless of the dose inhibited the development of the edema. Its effect was similar to that observed when the highest dose of L-NAME was administered. It may be that the non-selective blockade of cNOS by the highest dose of L-NAME also inhibited the iNOS pathway. CONCLUSION: Our data suggest that iNOS could be directly involved in pulmonary edema induced by vagotomy and cNOS appears to participate as a protector mechanism.
Subject(s)
Animals , Male , Rats , Nitric Oxide Synthase Type II/metabolism , Nitric Oxide Synthase Type III/metabolism , Nitric Oxide/metabolism , Pulmonary Edema/metabolism , Vagotomy/adverse effects , Enzyme Inhibitors/therapeutic use , Guanidines/therapeutic use , NG-Nitroarginine Methyl Ester/therapeutic use , Nitric Oxide Synthase Type II/antagonists & inhibitors , Nitric Oxide Synthase Type III/antagonists & inhibitors , Pulmonary Edema/drug therapy , Pulmonary Edema/etiology , Pulmonary Edema/prevention & control , Rats, Wistar , Severity of Illness Index , Time FactorsABSTRACT
OBJECTIVE@#To investigate the expression changes of aquaporins 1 (AQP1) in contused lung tissue of rats and its relationship with pulmonary edema.@*METHODS@#SD rats were randomly divided into experimental and control groups. The pulmonary contusion models were then prepared. The expression and distribution of AQP1 in lung tissue of the rats were detected by immunohistochemistry.@*RESULTS@#The lung tissue showed edema, hemorrhage, inflammatory cell infiltration 1 h, 3 h after pulmonary contusion, and the inflammatory response aggravated after 5 h. AQP1 expression at 1 h, 3 h and 5 h in the contusion group were significantly higher than that of the control group (P < 0.01). The expression of AQP1 continued to increase with time and aggravation of edema compared to the control group. AQP1 was mainly distributed in the capillary endothelial cells and interstitial cells of the bronchial and alveolar walls. Although there were no observed changes in AQP1 expression location in contused lung tissue, the intergrated optical density(IOD) showed significant statistical difference (P < 0.01).@*CONCLUSION@#There might exist an dysregulation of AQPs gene expression in contused lung tissue, leading to a large number of abnormal transmembrane water transportation and abnormal water accumulation, which may be one of the reasons for pulmonary edema in contused lung tissue.