2008 Volume 22 Issue 2 Pages 118-128
Rat air leak models were closured by fibrin glue, sheeted fibrin glue, and polyglycolic acid mesh combined with fibrin glue. The sealed sites including pleural surface were evaluated by both histology and ultra micromorphology. Adhesion between the sealed site and chest wall was observed for sheeted fibrin glue and polyglycolic acid mesh combined with fibrin glue, but not for fibrin glue. In all methods, fibroblast growth was observed on the pleural surface following air leak sealing, and angiogenesis was also observed when using sheeted fibrin glue and polyglycolic acid mesh combined with fibrin glue. Mesothelial cells were not observed using any method. In addition to inflammation, the pleural surface was thought to have thickened due to the extracellular matrix produced by the increased number of fibroblasts. In particular, when utilizing the polyglycolic acid mesh combined with fibrin glue, the thickening of the pleural surface was attributed to the transfer and migration of fibroblasts to the pleural defect, functioning of the applied polyglycolic acid mesh as a scaffold for cells, the subsequent involvement of growth factors in the body, and tissue remodeling due to the extracellular matrix produced by fibroblast cells. Sealant materials are reinforcement of the pleura by pleural thickening through a procedure similar to tissue engineering techniques. In conclusion, for development of the tissue adhesive, it is necessary improvement of the biocompatibility, control of the inflammation, prevention of the adhesion, to synchronize with the movement of lungs during respiration.