Objective:

Our aim is to investigate the role of HBO (hyperbaric oxygen), NAC (N-acetylcysteine), and HBO plus NAC on the necrosis area of random rat's skin flaps of a modified McFarlane flap design.

Materials and Methods:

Thirty-two male Wistar rats were randomly divided into four groups: G-S (sham: n = 8), G-NAC (NAC: n = 8), G-HBO (HBO: n = 8), and G-HN (HBO plus NAC: n = 8). A rectangular skin flap (2 × 8 cm2) was dissected from the muscular dorsal layer, preserving the cranial pedicle. Polyethylene film was placed over the muscular layer and an interrupted 3.0 nylon suture was employed to fix the flap into the original place. On the eighth day, full-thickness biopsy samples (2 × 1 cm2) were collected from the proximal, middle, and cranial areas of the skin flap, and in a site away from the flap labelled as the control area.

Results:

The measurements of necrotic areas in the groups were 18.3% in G-S, 24.3% in G-NAC, 12.6% in G-HBO, and 14.9% in G-HN. Significant difference was observed between the groups G-HBO and G-HN as well as G-NAC.

Conclusion:

HBO is associated with reduced area of necrosis of skin flap. The G-NAC group was associated with poor results when examined in isolation. The association between HBO and NAC did not produce favourable results with respect to the use of HBO alone. These findings suggest that the diffusion of oxygen through the interstitial space was the determining factor of more favourable results of HBO.

The thermally dimorphic fungus Paracoccidioides brasiliensis (Pb) is the causative agent of paracoccidioidomycosis (PCM), one of the most frequent systemic mycosis that affects the rural population in Latin America. PCM is characterized by a chronic inflammatory granulomatous reaction, which is consequence of a Th1-mediated adaptive immune response. In the present study we investigated the mechanisms involved in the immunoregulation triggered after a prior contact with cell-free antigens (CFA) during a murine model of PCM. The results showed that the inoculation of CFA prior to the infection resulted in disorganized granulomatous lesions and increased fungal replication in the lungs, liver and spleen, that paralleled with the higher levels of IL-4 when compared with the control group. The role of IL-4 in facilitating the fungal growth was demonstrated in IL-4-deficient- and neutralizing anti-IL-4 mAb-treated mice. The injection of CFA did not affect the fungal growth in these mice, which, in fact, exhibited a significant diminished amount of fungus in the tissues and smaller granulomas. Considering that in vivo anti-IL-4-application started one week after the CFA-inoculum, it implicates that IL-4-CFA-induced is responsible by the mediation of the observed unresponsiveness. Further, the characterization of CFA indicated that a proteic fraction is required for triggering the immunosuppressive mechanisms, while glycosylation or glycosphingolipids moieties are not. Taken together, our data suggest that the prior contact with soluble Pb antigens leads to severe PCM in an IL-4 dependent manner.