Wound tensile strength and contraction rate are not affected by laparotomy or pneumoperitoneum J. C. Wickens, R. L. Whelan, J. D. F. Allendorf, J. Donahue, E. Buxton, A. McKee, K. Panageas, N. Gleason, S. Lee, M. Bessler Department of Surgery, Columbia University and the Columbia-Presbyterian Medical Center, 161 Fort Washington Avenue, New York, NY 10032, USA Received: 26 September 1997/Accepted: 27 January 1998 Abstract Background: Many cellular elements responsible for wound healing are affected by laparotomy. The aim of this study was to evaluate the effects of laparotomy and CO 2 pneu- moperitoneum on wound healing. Methods: Male Sprague Dawley rats were randomly as- signed to one of three experimental groups. Anesthesia con- trol rats underwent no procedure. Pneumoperitoneum group rats were insufflated with CO 2 gas. Laparotomy group rats underwent a 7-cm midline laparotomy incision. The inter- ventions were 30 min long. For the incisional study (n  30), a 4-cm dorsal full-thickness skin incision was made on each rat and then closed with staples. On postoperative days 7 and 14, an equal number of rats were sacrificed from each group, and wound tensile strength measurements were per- formed. For the excisional study (n  45), each group of 15 rats underwent a 2-cm diameter circular dorsal full- thickness skin excision. Blinded measurements of wound area were performed every other day until wounds closed. Results: Wound tensile strength values were not signifi- cantly different among experimental groups at either time point. The study had a power of 80% to find a 30% differ- ence at POD 7 and a power of 80% to find a 23% difference at POD 14 to a confidence level of p < 0.05. Wound con- traction data from the excisional model were analyzed with the Generalized Estimation Equations statistical approach. When we modeled the treatment group as a covariate, no statistical difference was found between groups, demon- strating equal slopes across time. Conclusions: From the results of these studies, we conclude that wound healing in this model is not significantly dimin- ished following laparotomy or peritoneal insufflation, as compared to anesthesia control. Key words: Laparoscopy — Wound healing — Incision — Excision — Tensile strength — Rat Major surgery through a laparotomy incision is associated with a decrease in cell-mediated immune function that can last up to nine days [10, 12]. Decreases in the following parameters have been documented following open surgery: (a) lymphocyte and neutrophil chemotaxis, (b) natural killer cell activity, (c) lymphocyte and macrophage interactions, and (d) delayed-type hypersensitivity (DTH) responses [5, 10, 12, 14, 15]. Wound healing involves many of these cell types and might therefore also be adversely affected by laparotomy. The DTH response and wound healing both rely on the normal function of both macrophages and T cells. If the diminished postoperative DTH response seen after open surgery is due to altered macrophage or T-cell function, then the process of wound healing might be similarly affected. Macrophages secrete several cytokines that are essential to both the DTH response and to wound healing including platelet-derived growth factor (PDGF), tumor necrosis fac- tor  (TNF-), -interferon (IFN-), and transforming growth factor  (TGF-). Regan et al. demonstrated that macrophage depletion reduces wound breaking strength and is associated with decreased wound collagen content [3, 9]. Cytokines, including PDGF, TNF-, and TGF- can modu- late fibroblast function, which is essential for collagen de- position and wound tensile strength. Topical application of cytokines TGF- and PDGF to a healing wound has been shown to be associated with increased wound breaking strength [7, 13]. T-cell proliferation is also central to cell-mediated im- munity, the DTH response, and wound healing. Activated T cells proliferate and release cytokines that are responsible for the recruitment of macrophages, granulocytes, and ad- ditional T cells to the area of injury. Application of factors known to stimulate T-cell proliferation (growth hormone, vitamin A, arginine) have been shown to increase wound breaking strength and collagen content [6, 16, 17]. T-cell depletion has also been shown to reduce wound breaking strength and collagen content [3]. One purpose of our study was to determine if there were Correspondence to: M. Bessler Surg Endosc (1998) 12: 1166–1170 © Springer-Verlag New York Inc. 1998