Teixeira Lisete R, Vargas Francisco S, Acencio Milena M P, Paz Pedro F S, Antonangelo Leila, Vaz Marcelo A C, Marchi Evaldo
Laboratory of Pleura, Pulmonary Division, Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil.
Chest. 2005 Dec;128(6):4041-5. doi: 10.1378/chest.128.6.4041.
To determine whether the administration of antiinflammatory drugs interferes with experimental pleurodesis induced by silver nitrate or talc.
Two groups of 30 white New Zealand rabbits were scheduled to receive an intrapleural injection of 0.5% silver nitrate or 400 mg/kg of talc. Each group was further classified into three subgroups (10 animals each), which received the following: (subgroup 1) the sclerosing agent only, (subgroup 2) the sclerosing agent plus 1 mg/kg of methylprednisolone, and (subgroup 3) the sclerosing agent plus 1.1 mg/kg of diclofenac sodium. The antiinflammatory agents were administered IM 24 h before the sclerosing agent and daily during the first week, followed by once-weekly injections until death at 28 days. At this time, the pleural cavity was macroscopically evaluated, and samples of pleura and lungs were collected for further microscopic examination.
The degree of pleural adhesions was higher after silver nitrate administration (p = 0.019). No reduction in the adhesions was observed after administering antiinflammatory drugs to this group (p > 0.05). Conversely, the adhesion score was significantly reduced after administration of both prednisolone (p = 0.028) and diclofenac (p = 0.032) to the animals that received talc. Administration of the antiinflammatory agents did not influence microscopic pleural or lung changes induced by silver nitrate or talc.
These results show that the sustained systemic administration of antiinflammatory agents (steroidal or nonsteroidal) reduces the degree of pleural adhesions in animals with talc-induced pleurodesis but does not affect silver nitrate-induced pleurodesis. Extrapolation of these results to humans suggests that the use of antiinflammatory drugs should be avoided in patients with talc-induced pleurodesis and that appropriate clinical studies with silver nitrate should be conducted in patients chronically treated with these antiinflammatory agents.
确定抗炎药物的使用是否会干扰硝酸银或滑石粉诱导的实验性胸膜固定术。
两组，每组30只白色新西兰兔，计划接受胸膜腔内注射0.5%硝酸银或400mg/kg滑石粉。每组进一步分为三个亚组（每组10只动物），分别接受以下处理：（亚组1）仅硬化剂；（亚组2）硬化剂加1mg/kg甲泼尼龙；（亚组3）硬化剂加1.1mg/kg双氯芬酸钠。抗炎药物在硬化剂注射前24小时肌肉注射，在第一周每天注射，随后每周注射一次，直至28天处死。此时，对胸膜腔进行宏观评估，并采集胸膜和肺组织样本进行进一步显微镜检查。
硝酸银给药后胸膜粘连程度更高（p = 0.019）。该组给予抗炎药物后未观察到粘连减少（p > 0.05）。相反，接受滑石粉的动物给予泼尼松龙（p = 0.028）和双氯芬酸（p = 0.032）后粘连评分显著降低。抗炎药物的使用未影响硝酸银或滑石粉诱导的微观胸膜或肺部变化。
这些结果表明，持续全身给予抗炎药物（甾体或非甾体）可降低滑石粉诱导胸膜固定术动物的胸膜粘连程度，但不影响硝酸银诱导的胸膜固定术。将这些结果外推至人类表明，滑石粉诱导胸膜固定术的患者应避免使用抗炎药物，并且应对长期接受这些抗炎药物治疗的患者进行硝酸银的适当临床研究。
