Abstract
To assess the effect of prokinetic agents on abdominal wall wound healing in rats submitted to segmental colectomy and colonic anastomosis. Sixty rats were randomly allocated into three groups according to the agents they would receive in the postoperative period: M (metoclopramide); B (bromopride); and C (control, saline 0.9%). Surgical procedures were performed identically in all animals, and consisted of a midline laparotomy followed by resection of a 1-cm segment of large bowel with end-to-end anastomosis. The abdominal wall was closed in two layers with running stitches. Abdominal wall samples were collected on the 3rd or 7th postoperative day for measurement of breaking (tensile) strength and histopathological assessment. There were no statistically significant differences in tensile strength of the abdominal wall scar between groups M, B, and C, nor between the three and seven days after surgery subgroups. On histopathological assessment, there were no statistically significant between-group differences in collagen deposition or number of fibroblasts at the wound site Use of the prokinetic drugs metoclopramide or bromopride had no effect on abdominal wall healing in rats submitted to segmental colectomy and colonic anastomosis.
Highlights
Abdominal wall dehiscence and incisional hernia are the most common complications of surgical procedures that require laparotomy for access to the peritoneal cavity[1,2]
The 10-year prevalence of incisional hernia may be as high as 20%, and that of wound dehiscence, 0.2–11%; both complications are associated with adverse economic impact and worse patient quality of life[3,4]
The aim of this study was to assess the effect of two prokinetic agents—metoclopramide and bromopride—on abdominal wall healing in rats after colectomy and colonic anastomosis
Summary
Abdominal wall dehiscence and incisional hernia are the most common complications of surgical procedures that require laparotomy for access to the peritoneal cavity[1,2]. The 10-year prevalence of incisional hernia may be as high as 20%, and that of wound dehiscence, 0.2–11%; both complications are associated with adverse economic impact and worse patient quality of life[3,4]. The predominant cause of these complications is acute failure of the sequential, multifactorial process that leads to adequate wound healing[1,5]. The healing process begins with hemostasis[5,7]. This is followed by the inflammatory response, during which macrophages and polymorphonuclear neutrophils migrate from the circulation to the wound site in response to increasing cytokine levels[5,8]. Later stages include proliferation of blood vessels and fibroblasts with formation of granulation tissue, collagen synthesis, connective tissue remodeling, and acquisition of tensile strength[5,9]
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