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 fat tissue could induce neovascularization and produce cytokines related to tissue repair. Neovascularization was examined using chick chorioallantoic membranes. Pieces of pericardial fat tissue, omentum, and intercostal muscle were individually placed on a number of chorioallantoic membranes and neovascularization induced by each material was assayed 6 days after the implantation. The intensity of neovascularization was in the order of pericardial fat > or = 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 pericardial fat tissue. The latter was obtained 24 h after the addition of lipopolysaccharide (LPS) following various incubation times. All cytokines other than IFN gamma are known to play a part in tissue repair, whereas IFN gamma is negatively related to tissue repair because it inhibits fibroblast growth. The pericardial fat tissue incubated with LPS produced a certain amount of IL-1 on day 1, and TNF alpha on days 1 and 8, whereafter these values decreased to an undetectable level. Irrespective of the addition of LPS, a large amount of IL-6 was observed in the supernatant of pericardial fat tissue and it was detectable until day 29. On the contrary, INF gamma was not detected at any assay time. These observations suggest that a pericardial fat pad flap could possibly be beneficial in the prevention of bronchopleural fistula after pulmonary resection.