OBJECTIVE: Although fibrinogen- and thrombin-impregnated collagen (TachoSil; Takeda GmbH, Linz, Austria) can be applied to prevent air leakage, the impact of its use on lung healing is unknown. Therefore, we histologically evaluated the long-term healing process associated with the use of TachoSil to prevent air leakage in a canine model. METHODS: Via left thoracotomy, visceral pleural defects of 10 × 10 mm were created on each lung lobe of female beagles. After air leakage was confirmed, each pleural defect was covered with TachoSil. The repair sites were histologically evaluated on postoperative days 0, 4, 7, 14, 28, and 56. RESULTS: All animals survived, and none developed pneumothorax. Histologically, inflammatory cells infiltrated the TachoSil from the pleural defect, and pleural mesothelium comprised the regenerated outermost layer of the TachoSil soon after the surgery. Inflammatory cells, myofibroblasts, and neovascular vessels subsequently spread over the entire TachoSil. The number of inflammatory cells decreased, and myofibroblast and neovascular vessels replaced the entire TachoSil. In addition, the elastic layer started to regenerate from both edges and completely repaired the pleural defect. The lung parenchyma around the pleural defects was not influenced throughout the observational period, because these healing processes occurred only inside the TachoSil. CONCLUSIONS: TachoSil provided a mechanical scaffold on which healing could proceed, followed by biodegradation over the long term. TachoSil safely repaired the pleural defects without affecting lung parenchyma.
OBJECTIVE: Although fibrinogen- and thrombin-impregnated collagen (TachoSil; Takeda GmbH, Linz, Austria) can be applied to prevent air leakage, the impact of its use on lung healing is unknown. Therefore, we histologically evaluated the long-term healing process associated with the use of TachoSil to prevent air leakage in a canine model. METHODS: Via left thoracotomy, visceral pleural defects of 10 × 10 mm were created on each lung lobe of female beagles. After air leakage was confirmed, each pleural defect was covered with TachoSil. The repair sites were histologically evaluated on postoperative days 0, 4, 7, 14, 28, and 56. RESULTS: All animals survived, and none developed pneumothorax. Histologically, inflammatory cells infiltrated the TachoSil from the pleural defect, and pleural mesothelium comprised the regenerated outermost layer of the TachoSil soon after the surgery. Inflammatory cells, myofibroblasts, and neovascular vessels subsequently spread over the entire TachoSil. The number of inflammatory cells decreased, and myofibroblast and neovascular vessels replaced the entire TachoSil. In addition, the elastic layer started to regenerate from both edges and completely repaired the pleural defect. The lung parenchyma around the pleural defects was not influenced throughout the observational period, because these healing processes occurred only inside the TachoSil. CONCLUSIONS: TachoSil provided a mechanical scaffold on which healing could proceed, followed by biodegradation over the long term. TachoSil safely repaired the pleural defects without affecting lung parenchyma.