Pleurodesis is inhibited by anti-vascular endothelial growth factor antibody.

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.