New York, N.Y. From the Laboratory for Bioregenerative Medicine and Surgery, Department of Surgery, Weill Cornell Medical College.
Plast Reconstr Surg. 2010 Jun;125(6):1670-1678. doi: 10.1097/PRS.0b013e3181d4fdc5.
Ischemia-reperfusion injury is the propagation of injury following reintroduction of oxygen to previously ischemic tissue. The purpose of this study was to evaluate whether hydrogen sulfide provides protection against ischemia-reperfusion injury in enteric tissue.
In vitro (enterocyte anoxia-normoxia) and in vivo (rat intestinal ischemia-reperfusion) models of ischemia-reperfusion injury were tested with or without the addition of hydrogen sulfide. Apoptotic index was determined in vitro, and gross appearance, histology, and villus height (a measure of mucosal integrity) were assessed in vivo. Statistical analysis was performed, and significance was defined as p < 0.05.
In vitro, cells treated with 10 microM hydrogen sulfide after 1-hour anoxia experienced a significant decrease in apoptotic index compared with untreated control (0.5 +/- 0.3 percent versus 2.8 +/- 0.7 percent); after 3 hours of anoxia, cells treated with 1 microM, 10 microM, and 100 microM hydrogen sulfide experienced significant decreases in apoptotic index versus untreated control (1.6 +/- 0.8 percent, 1.8 +/- 0.9 percent, and 2.8 +/- 0.7 percent versus 8.6 +/- 1.7 percent). In vivo, intestine treated with [10 microM] or [100 microM] hydrogen sulfide retained normal coloration and villus architecture after 1-hour ischemia; after 2 hours of ischemia, only intestine treated with [10 microM] hydrogen sulfide appeared uninjured. After 1, 2, or 3 hours of ischemia, villus heights of intestine treated with [10 microM] or [100 microM] hydrogen sulfide were significantly higher than heights of non-hydrogen sulfide-treated villi.
Hydrogen sulfide significantly attenuates ischemia-reperfusion injury in intestinal tissue in vitro and in vivo. These results have significant implications for enteric free tissue transfers and other gastrointestinal procedures in which ischemic intervals may be anticipated.
再灌注损伤是指氧重新引入先前缺血组织时损伤的传播。本研究旨在评估硫化氢是否对肠组织的再灌注损伤提供保护。
采用体外（肠上皮细胞缺氧-复氧）和体内（大鼠肠缺血-再灌注）模型进行再灌注损伤试验，分别加入和不加入硫化氢。体外测定细胞凋亡指数，体内评估大体外观、组织学和绒毛高度（黏膜完整性的指标）。进行统计学分析，定义显著性差异为 p<0.05。
体外，1 小时缺氧后用 10 μM 硫化氢处理的细胞与未处理的对照组相比，凋亡指数显著降低（0.5±0.3%对 2.8±0.7%）；3 小时缺氧后，用 1 μM、10 μM 和 100 μM 硫化氢处理的细胞与未处理的对照组相比，凋亡指数显著降低（1.6±0.8%、1.8±0.9%和 2.8±0.7%对 8.6±1.7%）。体内，用[10 μM]或[100 μM]硫化氢处理的肠段在 1 小时缺血后保持正常色泽和绒毛结构；2 小时缺血后，只有用[10 μM]硫化氢处理的肠段看起来未受伤。1、2 或 3 小时缺血后，用[10 μM]或[100 μM]硫化氢处理的肠段的绒毛高度明显高于未用硫化氢处理的绒毛高度。
硫化氢可显著减轻肠组织体外和体内的再灌注损伤。这些结果对肠游离组织移植和其他可能需要缺血间隔的胃肠道手术具有重要意义。
