The Length of Surgical Skin Incision in Postoperative Inflammatory Reaction

Abstract

Background and objectives: Surgery provokes inflammatory and immune responses, so efforts have been made to reduce host response by using less invasive techniques. The purpose of this experimental study was to investigate the surgical stress induced by skin incision and the role of liver response in this process.

Methods: Seventy male anesthetized Wistar rats were subjected to a midline incision confined strictly to the skin (dermis) of either 1 cm long (n = 20), 10 cm long (n = 20), or no incision (n = 20) or served as controls (n = 10). Skin trauma was left open for a 20-minutes period, and then was meticulously sutured. At 3 and 24 hours later, laparotomy was performed on half the rats of each group, for blood and liver sampling. In serum and liver homogenates, cytokine-induced neutrophil chemoattractant (CINC)1/interleukin (IL)-8 and tumor necrosis factor (TNF)-α levels were measured with enzyme-linked immunosorbent assays and nitric oxide (NO) using a Griess reaction.

Results: Skin trauma was found to significantly (P < .01) increase all inflammatory mediators tested (CINC1/IL-8, TNF-α, NO) in serum of operated rats versus controls, the increase being proportionally dependent on the length of skin incision. In liver homogenates, CINC1/IL-8 was significantly (P < .01) increased in operated animals versus controls, similarly to serum levels. In contrast, liver TNF-α levels were inversely related to serum levels, and a significant (P < .01) decrease in TNF-α was observed in liver homogenates of operated animals compared with the controls, indicating that the increased TNF-α in blood reflects liver TNF-α secretion.

Conclusion: Our findings suggest that inflammatory and immune reactions induced by skin-only surgical trauma are closely correlated to the length of skin incision.

Keywords: Postoperative immune reaction; Skin stress response; Surgical incision; Surgical skin trauma.

Figure 1.

Flowchart of the in vivo experiments.

Figure 2.

Serum CINC1/IL-8 levels. Data are presented as the mean ± standard error (SE) of 10 samples per group. C0 represents baseline measurements; C3 and C24 represent anesthesia-only subjected rats, at 3 and 24 hours; L3 and L24 represent the long-incision–subjected rats at 3 and 24 hours; and S3 and S24 represent the short-incision–subjected rats at 3 and 24 hours.

Figure 3.

Serum TNF-α levels. Data are presented as the mean ± standard error (SE) of 10 samples per group. C0 represents baseline measurements; C3 and C24 represent anesthesia-only subjected rats, at 3 and 24 hours; L3 and L24 represent the long-incision–subjected rats at 3 and 24 hours; and S3 and S24 represent the short-incision–subjected rats at 3 and 24 hours.

Figure 4.

Serum NO levels. Data are presented as the mean ± standard error (SE) of 10 samples per group. C0 represents baseline measurements; C3 and C24 represent anesthesia-only subjected rats, at 3 and 24 hours; L3 and L24 represent the long-incision–subjected rats at 3 and 24 hours; and S3 and S24 represent the short-incision–subjected rats at 3 and 24 hours.

Figure 5.

Liver homogenates CINC1/IL-8 levels. Data are presented as the mean ± standard error (SE) of 10 samples per group. C0 represents baseline measurements; C3 and C24 represent anesthesia-only subjected rats, at 3 and 24 hours; L3 and L24 represent the long-incision–subjected rats at 3 and 24 hours; and S3 and S24 represent the short-incision–subjected rats at 3 and 24 hours.

Figure 6.

Liver homogenate TNF-α levels. Data are presented as the mean ± standard error (SE) of 10 samples per group. C0 represents baseline measurements; C3 and C24 represent anesthesia-only subjected rats, at 3 and 24 hours; L3 and L24 represent the long-incision–subjected rats at 3 and 24 hours; and S3 and S24 represent the short-incision–subjected rats at 3 and 24 hours.