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Effects of pneumonectomy on nitric oxide synthase expression and perivascular edema in the remaining lung of rats

机译:肺切除术对大鼠剩余肺中一氧化氮合酶表达和血管周水肿的影响

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Pneumonectomy is associated with high mortality and high rates of complications. Postpneumonectomy pulmonary edema is one of the leading causes of mortality. Little is known about its etiologic factors and its association with the inflammatory process. The purpose of the present study was to evaluate the role of pneumonectomy as a cause of pulmonary edema and its association with gas exchange, inflammation, nitric oxide synthase (NOS) expression and vasoconstriction. Forty-two non-specific pathogen-free Wistar rats were included in the study. Eleven animals died during or after the procedure, 21 were submitted to left pneumonectomy and 10 to sham operation. These animals were sacrificed after 48 or 72 h. Perivascular pulmonary edema was more intense in pneumonectomized rats at 72 h (P = 0.0131). Neutrophil density was lower after pneumonectomy in both groups (P = 0.0168). There was higher immunohistochemical expression of eNOS in the pneumonectomy group (P = 0.0208), but no statistically significant difference in the expression of iNOS. The lumen-wall ratio and pO2/FiO2 ratio did not differ between the operated and sham groups after pneumonectomy. Left pneumonectomy caused perivascular pulmonary edema with no elevation of immunohistochemical expression of iNOS or neutrophil density, suggesting the absence of correlation with the inflammatory process or oxidative stress. The increased expression of eNOS may suggest an intrinsic production of NO without signs of vascular reactivity.
机译:肺切除术与高死亡率和高并发症发生率相关。肺切除术后肺水肿是导致死亡的主要原因之一。关于其病因和与炎症过程的关系知之甚少。本研究的目的是评估肺切除术作为肺水肿的原因及其与气体交换,炎症,一氧化氮合酶(NOS)表达和血管收缩的关系。该研究包括42只非特异性无病原体的Wistar大鼠。在手术过程中或手术后有11只动物死亡,其中21例接受了左肺切除术,10例进行了假手术。在48或72小时后将这些动物处死。肺切除术大鼠在72 h时血管周围肺水肿更为严重(P = 0.0131)。两组在肺切除术后中性粒细胞密度均较低(P = 0.0168)。肺切除术组中eNOS的免疫组织化学表达较高(P = 0.0208),但iNOS的表达无统计学差异。手术组和假手术组在肺切除后的管壁比和pO2 / FiO2比没有差异。左肺切除术引起血管周围肺水肿,iNOS的免疫组织化学表达或中性粒细胞密度均未升高,提示与炎症过程或氧化应激无关。 eNOS的表达增加可能暗示了NO的内在产生,而没有血管反应的迹象。

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