Dubaybo B A, Bayasi G, Rubeiz G J
Division of Pulmonary and Critical Care Medicine, Veterans Administration Medical Center, Detroit, Mich, USA.
J Thorac Cardiovasc Surg. 1995 Aug;110(2):396-404. doi: 10.1016/S0022-5223(95)70236-9.
So that changes in production and binding of tumor necrosis factor-alpha during postpneumonectomy lung growth could be determined, rats underwent left lung resection and were killed 3, 7, or 14 days later, 1 hour after the injection of 3H-thymidine. Serum was collected, and the lungs were lavaged and perfused in vitro. Lung volumes were measured. Lungs were homogenized, and changes in lung weight, protein content, deoxyribonucleic acid content, deoxyribonucleic acid synthesis, and tyrosine kinase activity of different lobes were recorded. Tumor necrosis factor-alpha content of serum, lavage fluid, and perfusate was measured by an enzyme-linked immunoassay. The binding of tumor necrosis factor-alpha to membrane extracts of lung homogenates was measured by immunoblots. Whereas the cardiac lobe of the remaining right lung demonstrated larger increases in size than other lobes after pneumonectomy, there was no difference in any growth parameter between it and the other lung lobes. Serum tumor necrosis factor-alpha was detectable in sham-operated animals and increased significantly after pneumonectomy. However, by day 14, it was not different from the level in sham-operated animals. In contrast, tumor necrosis factor-alpha in lavage fluid remained significantly elevated, and its binding increased gradually throughout the study period. Tumor necrosis factor-alpha in perfusate did not demonstrate any rise. We conclude that lung growth after pneumonectomy is uniform among various lobes, which suggests that it is regulated by humoral factors. Because tumor necrosis factor-alpha, a cytokine known to stimulate cellular proliferation and matrix synthesis, is produced and bound to the lung during this process, it may be one of the humoral factors implicated in postpneumonectomy lung growth.
为了确定肺切除术后肺生长过程中肿瘤坏死因子-α的产生和结合变化，对大鼠进行左肺切除，在注射³H-胸腺嘧啶核苷1小时后，于术后3、7或14天处死大鼠。收集血清，对肺进行体外灌洗和灌注。测量肺体积。将肺匀浆，记录不同肺叶的肺重量、蛋白质含量、脱氧核糖核酸含量、脱氧核糖核酸合成及酪氨酸激酶活性的变化。采用酶联免疫吸附测定法测量血清、灌洗液和灌注液中肿瘤坏死因子-α的含量。通过免疫印迹法测量肿瘤坏死因子-α与肺匀浆膜提取物的结合。肺切除术后，剩余右肺的心叶比其他肺叶体积增大更明显，但在心叶与其他肺叶之间，任何生长参数均无差异。在假手术动物中可检测到血清肿瘤坏死因子-α，肺切除术后其显著升高。然而，到第14天时，其水平与假手术动物无异。相比之下，灌洗液中的肿瘤坏死因子-α仍显著升高，且在整个研究期间其结合逐渐增加。灌注液中的肿瘤坏死因子-α未出现任何升高。我们得出结论，肺切除术后肺的生长在各肺叶之间是均匀的，这表明它受体液因子调节。由于肿瘤坏死因子-α这种已知可刺激细胞增殖和基质合成的细胞因子在此过程中产生并与肺结合，它可能是参与肺切除术后肺生长的体液因子之一。
