USE OF A PERICARDIAL FAT PAD FLAP FOR PREVENTING BRONCHOPLEURAL FISTULA - AN EXPERIMENTAL-STUDY FOCUSING ON THE ANGIOGENESIS AND CYTOKINE PRODUCTION OF THE FAT PAD

An experimental study was conducted to determine whether pericardial f at tissue could induce neovascularization and produce cytokines relate d to tissue repair. Neovascularization was examined using chick chorio allantoic membranes, Pieces of pericardial fat tissue, omentum, and in tercostal muscle were individually placed on a number of chorioallanto ic membranes and neovascularization induced by each material was assay ed 6 days after the implantation. The intensity of neovascularization was in the order of pericardial fat greater than or equal to omentum > muscle. Cytokines, such as interleukin 1 (IL-1) alpha and beta, tumor necrosis factor-alpha (TNF alpha), interferon-gamma (IFN-gamma), and interleukin 6 (IL-6) were assayed in a culture supernatant of pericard ial fat tissue. The latter was obtained 24 h after the addition of lip opolysaccharide (LPS) following various incubation times. All cytokine s other than IFN gamma are known to play a part in tissue repair, wher eas IFN gamma is negatively related to tissue repair because it inhibi ts fibroblast growth. The pericardial fat tissue incubated with LPS pr oduced a certain amount of IL-1 on day 1, and TNF alpha on days I and 8, whereafter these values decreased to an undetectable level. Irrespe ctive of the addition of LPS, a large amount of IL-6 was observed in t he supernatant of pericardial fat tissue and it was detectable until d ay 29. On the contrary, INF gamma was not detected at any assay time. These observations suggest that a pericardial fat pad flap could possi bly be beneficial in the prevention of bronchopleural fistula after pu lmonary resection.