Parenchymal cytokine expression precedes clinically observed ischemia in dorsal flaps in the rat.
Cytokines have been implicated as pivotal mediators of the wound-healing process. An understanding of the production and interaction of cytokines may lead to a better appreciation of the complex mechanisms of flap ischemia. The potential would then exist for novel diagnostic and therapeutic approaches to prevent and reverse damage to the endangered flap. The goal of this study was to determine the expression of parenchymal cytokines at various time points during flap ischemia. Punch biopsies were obtained from McFarlane dorsal flaps in the Sprague-Dawley murine model. We examined cytokine mRNA profiles for interleukin 1 alpha (IL-1 alpha), IL-2, IL-6, basic fibroblast growth factor (b-FGF), gamma-interferon (gamma IFN), transforming growth factor beta (TGF-beta), and platelet-derived growth factor A chain (PDGF-alpha) using in situ hybridization. Samples were taken from 0 to 48 hours postoperatively, with n = 3 for each time point. Eight hours postoperatively there was an abrupt peak of parenchymal cytokine expression at the bases of the flaps. Clinically at this time the flaps appeared completely viable without evidence of ischemic change. Leukocyte cytokine production peaked at 16 hours, when distal flap ischemia was evident clinically. These findings demonstrate an early peak of cytokine expression prior to clinical evidence of ischemia.
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Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Calif., USA.
Hoyt
J
J
Sibley
R K
RK
Press
B H
BH
D000818:Animals; D016207:Cytokines / Q000378:metabolism*; D016222:Fibroblast Growth Factor 2 / Q000378:metabolism; D007511:Ischemia / Q000503:physiopathology*; D011183:Postoperative Complications / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013524:Surgical Flaps / Q000502:physiology*; D013997:Time Factors; D014945:Wound Healing / Q000502:physiology*
D016207:Cytokines; D016222:Fibroblast Growth Factor 2