Nitric oxide modulates metalloproteinase-2, collagen deposition and adhesion rate after polypropylene mesh implantation in the intra-abdominal wall.

Prosthetic meshes are commonly used to correct abdominal wall defects. However, the inflammatory reaction induced by these devices in the peritoneum is not completely understood. We hypothesized that nitric oxide (NO), produced by nitric oxide synthase 2 (NOS2) may modulate the response induced by mesh implants in the abdominal wall and, consequently, affect the outcome of the surgical procedure. Polypropylene meshes were implanted in the peritoneal side of the abdominal wall in wild-type and NOS2-deficient (NOS2(-/-)) mice. After 15 days tissues around the mesh implant were collected, and inflammatory markers (the cytokine interleukin 1ß (IL-1ß) and NO) and tissue remodeling (collagen and metalloproteinases (MMP) 2 and 9) were analyzed. The lack of NOS2-derived NO induced a higher incidence of visceral adhesions at the mesh implantation site compared with wild-type mice that underwent the same procedure (P<0.05). Additionally, higher levels of IL-1ß were present in the mesh-implanted NOS2(-/-) animals compared with control and wild-type mice. Mesh implantation induced collagen I and III deposition, but in smaller amounts in NOS2(-/-) mice. MMP-9 activity after the surgical procedure was similarly increased in both groups. Conversely, MMP-2 activity was unchanged in mesh-implanted wild-type mice, but was significantly increased in NOS2(-/-) mice (P<0.01), due to decreased S-nitrosylation of the enzyme in these animals. We conclude that NOS2-derived NO is crucial for an adequate response to and integration of polypropylene mesh implants in the peritoneum. NO deficiency results in a prolonged inflammatory reaction to the mesh implant, and reduced collagen deposition may contribute to an increased incidence of visceral adhesions.

Use of chitosan membrane associated with polypropylene mesh to prevent peritoneal adhesion in rats.

The correction of wall abdominal defects often requires the use of implants such as polypropylene meshes. In spite of presenting good tissue acceptance, these biomaterials can migrate to adjacent viscera, promote enterocutaneos fistulas, tissue adherence and visceral erosions. In this work, the barrier effect of chitosan films associated with polypropylene meshes on adhesion formation experimentally induced in Wistar rats was evaluated. The animals were divided into two groups with 10 animals each. Animals in the CPP group were implanted with chitosan films associated with polypropylene meshes, whereas the ones in the PP group received only polypropylene meshes. After 8 days, the animals were submitted to euthanasia using CO(2) and a descriptive study focusing adhesion formation, visceral involvement with sutures and mesh peritonization was performed. Also, subimplanted material was collected for histopathology analysis. The results showed that the CPP group presented weak adhesions to the omentum over the stitch knots in eight animals. In all animals, the meshes were peritonized, not allowing their visualization after removing the chitosan films. In the PP group, six animals presented intestinal adhesions to the meshes and, in one of them, hepatic adhesion to the mesh was observed, besides omentum adhesion on more than 50% of the mesh area. The protective effect of chitosan films when sutured over polypropylene meshes, as well as no exacerbation of inflammation associated to the peritoneal lesions was statistically demonstrated. Therefore, chitosan films can indeed minimize the formation of peritoneal adhesions induced by polypropylene meshes in rats.