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Background and Objective: The mechanism by which iodopovidone achieves pleurodesis is unknown. This study investigated whether iodopovidone is as effective as doxycycline in producing pleurodesis and whether systemic corticosteroids diminish its efficacy., Methods: Four groups of seven New Zealand rabbits were assigned to the following intrapleural treatment groups: 2 mL of 2% iodopovidone, 2 mL of 4% iodopovidone, 2 mL of 4% iodopovidone plus 0.8 mg/kg triamcinolone intramuscularly weekly and 10 mL/kg doxycycline in 2 mL. Pleural fluid was collected 24, 48 and 72 h after intrapleural injections and analysed for WCC, protein and LDH levels. The rabbits were killed 2 weeks after the injections. Pleurodesis was graded macroscopically on a scale from 1 to 8. The degree of microscopic pleural fibrosis and pleural inflammation was graded from the HE stain slides., Results: The mean volume of pleural fluid as well as the mean total WCC was significantly lower in the steroid-treated group than in the other groups. The degree of the resulting pleurodesis was similar in the 2% iodopovidone (7.00 +/- 1.29), 4% iodopovidone (7.71 +/- 0.76) and doxycycline (7.14 +/- 0.90) groups (P > 0.05) whereas the pleurodesis score of the steroid group (3.71 +/- 1.98) was significantly lower than all other groups (P < 0.05). The degree of microscopic pleural fibrosis and pleural inflammation was significantly lower in the steroid group than in the 2% iodopovidone or 4% iodopovidone group., Conclusions: Both 2% and 4% iodopovidone can induce pleurodesis as efficaciously as doxycycline in rabbits. Systemic corticosteroids significantly decrease the efficacy of iodopovidone in producing pleurodesis.

Study Objectives: The intrapleural injection of transforming growth factor (TGF)-beta2 produces pleurodesis in rabbits associated with large pleural effusions. This study investigated whether anti-vascular endothelial growth factor (VEGF) antibody has any effect on the fluid production or the pleurodesis induced by TGF-beta2., Interventions and Measurements: Three groups of seven New Zealand white rabbits were administered TGF-beta2 5.0 microg intrapleurally. Two groups received anti-VEGF antibody (10 mg/kg and 25 mg/kg) IV 24 h before TGF-beta2 injection, and the third group received no antibody. The rabbits were killed at 2 weeks, and the macroscopic pleurodesis score was determined. The degree of pleural angiogenesis was assessed by immunohistochemical staining for factor VIII., Results: The administration of anti-VEGF antibodies had no significant effect on the pleural fluid volume or the characteristics of the fluid. The mean pleurodesis score of the seven rabbits in the control group (7.71 +/- 0.76) was significantly (p < 0.05) higher than that for seven rabbits in the low-dose treatment group (4.43 +/- 2.37) and the seven rabbits in the high-dose treatment group (4.57 +/- 2.36) [+/- ]. The percentage of pleural tissue demonstrating angiogenesis in the control group (4.87 +/- 0.43%) was significantly (p < 0.05) higher than that for the low-dose (2.94 +/- 0.68%) or high-dose (2.67 +/- 0.64%) antibody groups. When all rabbits were considered, there was a highly significant correlation between the pleural vascular density scores and the pleurodesis scores (r = 0.84, p < 0.01)., Conclusion: VEGF and angiogenesis appear to play a pivotal role in the production of a pleurodesis.

Study Objective: The aim of this study was to examined whether transforming growth factor (TGF)-beta(3) induces pleurodesis in rabbits and collagen production by human pleural mesothelial cells in vitro., Design: A combined animal and in vitro study., Methods: TGF-beta(3) was injected intrapleurally in rabbits at the following doses: 0.167 mug, 0.5 mug, 1.67 mug, and 5 mug (five rabbits per group). The rabbits were killed 14 days following injection, and pleurodesis was graded from 1 (none) to 8 (complete symphysis). Pleural mesothelial cell cultures were established from benign pleural effusions and treated with TGF-beta(3) for 48 h at the following doses: 0 (control), 5 ng/mL, 1.5 ng/mL, 5 ng/mL, and 15 ng/mL and 50 ng/mL (two independent experiments). Collagen I messenger RNA (mRNA) expression was quantified using real-time polymerase chain reaction., Results: The median pleurodesis score was 5 (interquartile range [IQR], 4.5) in the 0.167-mug group, 6 (IQR, 5) in the 0.5-mug group, 8 (IQR, 1) in the 1.67-mug group, and 8 (IQR, 0.5) in the 5-mug group (p = 0.012). Higher TGF-beta(3) doses induced the production of significantly more pleural fluid than the lower doses (p = 0.005). The pleural fluid induced by higher doses contained significantly lower numbers of nucleated cells (p = 0.014) and lactate dehydrogenase levels (p = 0.013) than the pleural fluid induced by lower doses of the agent. TGF-beta(3) markedly enhanced collagen I mRNA expression by the human pleural mesothelial cells. This effect peaked at 5 ng/mL TGF-beta(3). With this dose of TGF-beta(3), the collagen I mRNA expression was increased 16-fold over control levels., Conclusion: TGF-beta(3) causes a dose-dependent pleurodesis when administered intrapleurally in rabbits, and induces collagen messenger RNA synthesis from human pleural mesothelial cells.