Retraction and fibroplasia in a polypropylene prosthesis: experimental study in rats.

BACKGROUND: The treatment of hernia, independent of anatomical site and technique utilized, generally involves using prostheses, which may cause complications, despite their unarguable advantage in allowing safe reinforcement. An example of this is possible retraction, which causes discomfort and hernia recurrence. Polypropylene is still the most often used biomaterial of the great number available. The purpose of this study is to evaluate the amount of retraction of the polypropylene mesh, as well as the histological reactions that accompany this phenomenon. METHODS: Polypropylene meshes (Marlex) were inserted in an anterior position to the whole abdominal aponeurosis of 25 Wistar rats (Rattus norvegicus albinus). The animals were divided into groups and another intervention was performed 7, 28, and 90 days later to measure the dimensions of the prostheses and to calculate the final area. Histological analysis was performed with hematoxylin-eosin to evaluate neutrophils, macrophages, giant cells, and lymphocytes surrounding the mesh threads in ten random fields of each slide. RESULTS: Seven days after the mesh was inserted, the mean rate of retraction was 1.75% (P = 0.64); at 28 days, it was 3.75% (P = 0.02); and at 90 days, it was 2.5% (P = 0.01). As to the histological analysis, there was a total decline of neutrophils and a progressive increase of macrophages, giant cells, and lymphocytes proportional to the post-implant time of the mesh (P < 0.05). CONCLUSION: There was a statistically significant retraction of 3.75% at 28 days and 2.5% at 90 days after the prosthesis was inserted. There is a well-established sequence of cellular events which aim at synthesizing new connective tissue to reinforce the mesh.

Effects of N-acetylcysteine in hepatic ischemia-reperfusion injury during hemorrhagic shock.

This article seeks to standardize an experimental model of liver ischemia-reperfusion in rats following hemorrhagic shock modulated by N-acetylcysteine (NAC). Twenty-seven adult Wistar rats were randomized into three groups: the HS-IR-Garm underwent hemorrhagic shock with selective hepatic ischemia followed by reperfusion; the HSIR + NAC-G, the same procedure plus NAC; and the control group, only venous catheterization. Blood was withdrawn for 10 minutes until MABP reached 35 mm Hg, which was maintained for 1 hour. The blood was then reinjected as required to maintain MABP at that level. Ringer's lactate solution was infused in a volume equivalent to three times the shed blood, over a period of 15 minutes. Half of the shed blood was reinfused over 5 minutes. HSIR + NAC-G received 150 mg/kg of NAC, during treatment of the shock, and again 10 minutes before reperfusion and continued for 30 minutes. Finally, both groups were subjected to 40 minutes of warm selective hepatic ischemia and reperfusion for 1 hour. Data were analyzed by nonparametric tests (P < or =.05). Liver enzyme levels were higher in HS-IR-G (DHL = 6094 +/- 1688, AST = 746 +/- 175, and ALT = 457 +/- 90) than in HSIR + NAC-G group (DHL = 2920 +/- 284, AST = 419 +/- 113, and ALT = 253 +/- 26). The values in the control group were lower than both experimental groups (DHL = 965 +/- 173, AST = 163 +/- 42, and ALT = 82 +/- 28). Our data showed that liver ischemia-reperfusion injury following hemorrhagic shock produces important hepatic damage and that NAC reduces injury in this rat model.