Zhang Feng, Hu Eric C, Gerzenshtein Jacob, Lei Man-Ping, Lineaweaver William C
Division of Plastic Surgery, University of Mississippi Medical Center, Jackson, MS 39216, USA.
Ann Plast Surg. 2005 Mar;54(3):313-7.
Ischemic-reperfusion injury mediated by free radicals and neutrophils is the principal pathway for tissue injury and death. Cytokines influence activity of various cell types during the inflammatory process. In this study, expression of selected proinflammatory cytokines was examined in primary and secondary ischemia in the rat gracilis flap model. Sixty Sprague-Dawley rats were used in the study. Primary ischemia of each gracilis flap was induced by clamping its vascular pedicle for 1 hour. The flap was then replaced and allowed to reperfuse. Twenty-four hours later, a secondary ischemia was induced via vascular clamping for 4 hours. All muscle flaps were biopsied at 4 hours and 18 hours after primary ischemia. After secondary ischemia, each flap was biopsied immediately postevent, at 4 hours, and at 18 hours. Expression of tumor necrosis factor (TNF-alpha), interleukin (IL-1beta), and platelet-derived growth factor (PDGF) mRNA was determined by RT-PCR in each case. An equal sample size of gracilis muscle flaps, elevated in an identical fashion but not subjected to vascular clamping, was examined for baseline gene expression. Results showed that TNF-alpha gene expression was significantly up-regulated at 18 hours after secondary ischemia. IL-1 gene expression was up-regulated at 4 hours after primary ischemia, and was greatest at 4 hours after secondary ischemia. PDGF expression was up-regulated immediately after secondary ischemia, then at 4 hours after secondary ischemia (P < 0.05), and down-regulated during reperfusion. This study delineated changes in the expression of TNF-alpha, IL-1beta, and PDGF mRNA, in both primary and secondary ischemia and reperfusion episodes at several critical time points.
由自由基和中性粒细胞介导的缺血再灌注损伤是组织损伤和死亡的主要途径。细胞因子在炎症过程中影响各种细胞类型的活性。在本研究中，在大鼠股薄肌皮瓣模型的原发性和继发性缺血中检测了选定促炎细胞因子的表达。该研究使用了60只Sprague-Dawley大鼠。通过夹闭每只股薄肌皮瓣的血管蒂1小时诱导原发性缺血。然后将皮瓣复位并使其再灌注。24小时后，通过血管夹闭4小时诱导继发性缺血。在原发性缺血后4小时和18小时对所有肌皮瓣进行活检。继发性缺血后，在事件发生后立即、4小时和18小时对每个皮瓣进行活检。在每种情况下通过逆转录聚合酶链反应（RT-PCR）测定肿瘤坏死因子（TNF-α）、白细胞介素（IL-1β）和血小板衍生生长因子（PDGF）mRNA的表达。检查了同等样本量的以相同方式抬高但未进行血管夹闭的股薄肌皮瓣的基线基因表达。结果显示，继发性缺血后18小时TNF-α基因表达显著上调。IL-1基因表达在原发性缺血后4小时上调，在继发性缺血后4小时最高。PDGF表达在继发性缺血后立即上调，然后在继发性缺血后4小时上调（P<0.05），并在再灌注期间下调。本研究描绘了在几个关键时间点原发性和继发性缺血及再灌注发作期间TNF-α、IL-1β和PDGF mRNA表达的变化。
