PHARMACOLOGICAL ALTERATION OF THE LUNG VASCULAR-RESPONSE TO RADIATION
PHARMACOLOGICAL ALTERATION OF THE LUNG VASCULAR-RESPONSE TO RADIATION
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DOI：
10.1016/0360-3016(90)90541-q
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发表时间：
1990-08-01
影响因子：
7
通讯作者：
RASEY, JS
中科院分区：
文献类型：
--
作者：
GRAHAM, MM;EVANS, ML;RASEY, JS
本文研究了内皮细胞损伤在放射性肺损伤中的作用。血管通透性-表面积乘积（PS）被测量作为暴露于单剂量半胸照射的大鼠肺中内皮细胞损伤程度的指标。选择半胸照射来模拟临床放射治疗，其中仅照射肺的一部分。此外，它还提供了一个对照肺，以与辐照肺进行比较。辐射被假定为导致几种不同的生化途径的激活，从而导致肺损伤和纤维化。这些途径中的许多可以用药物特异性地阻断。研究了13种药物。地塞米松、吲哚美辛、克罗美辛、赛庚啶、维生素D3、茶碱和乙胺嗪均能有效降低照射侧肺PS。地塞米松，维生素D3和吲哚美辛也显着降低肺PS在未照射的肺和假照射大鼠。卡托普利、眼镜蛇毒因子、青霉胺、曲匹地尔、ε-氨基己酸、氨苯砜对半胸照射后肺PS无明显影响。我们的结论是，在早期辐射后肺损伤的主要途径涉及前列腺素，白三烯，组胺释放的巨噬细胞和肥大细胞。补体激活、蛋白水解酶和中性粒细胞迁移似乎不是辐射后早期肺损伤的重要介质。
The role of endothelial cell damage in the development of radiation injury in the lung was investigated in rats. Vascular permeability-surface area product (PS) was measured as an indicator of the degree of endothelial cell damage in lungs of rats exposed to single dose hemithorax irradiation. Hemithorax irradiation was chosen to simulate clinical radiotherapy, in which only a portion of the lung is irradiated. In addition, it provided a control lung to compare to the irradiated lung. Radiation is postulated to lead to activation of several different biochemical pathways that result in lung injury and fibrosis. Many of these pathways can be specifically blocked with drugs. Thirteen different drugs were studied. Dexamethasone, indomethacin, cromolyn, cyproheptadine, Vitamin D3, theophylline, and diethylcarbamazine were all effective at reducing lung PS on the irradiated side. Dexamethasone, Vitamin D3, and indomethacin also significantly reduced lung PS in the unirradiated lungs and in sham-irradiated rats. Captopril, cobra venom factor, penicillamine, trapidil, epsilon-amino caproic acid, an dapsone had no significant effect on lung PS after hemithorax irradiation. We conclude that the major pathways involved in early postradiation lung injury involve prostaglandin, leukotriene, and histamine release from macrophages and mast cells. Complement activation, proteolytic enzymes, and neutrophil migration do not seem to be important mediators of early postradiation lung injury.