The intrapleural injection of transforming growth factor-beta2 (TGF-β2) produces excellent pleurodesis in rabbits. However, a large transient pleural effusion, induced by the TGF-β2 and possibly mediated by the vascular endothelial growth factor (VEGF) is observed the first 48 hours after the injection and may intervene with the pleurodesis. The aim of this study was to investigate whether VEGF inhibitor has any effect on the fluid production or the the pleurodesis induced by TGF-β in rabbits.
Three groups of 7 New Zealand White rabbits were given TGF- β2 5.0 micrograms intrapleurally after chest tube placement. One group received 25 mg/kg anti-VEGF antibody IV, one group received 10 mg/kg anti-VEGF antibody IV and the third group served as the control. Pleural fluid was collected at 24 h, 48h and 72h after TGF-β2 injection. White blood cells (WBC) count, protein and LDH in the pleural fluids were measured and pleurodesis scores were evaluated after sacrificing the rabbits at 2 weeks.
There were no significant difference between the control group and two treatment groups for pleural fluid volume, WBC, protein, or LDH level. However, the treatment groups had significantly lower pleurodesis scores. The pleurodesis scores of control group was 7.71 ± 0.76 (mean ± SD), for low dose treatment group was 4.43 ± 2.37 and for high dose treatment group was 4.57±2.36.CONCLUSIONS: Anti-VEGF antibody partially blocks the pleurodesis induced by the TGFbeta2 in rabbits suggesting that VEGF plays a pivotal role in the production of a pleurodesis.
Pleurodesis may not be effective in pleural effusion patients treated with novel anti-angiogenic regimens that block VEGF.
Y. Guo, None.