Salerno G M, McBride D M, Bleicher J N
Division of Plastic and Reconstructive Surgery, Creighton University School of Medicine, Omaha, NE 68131.
Ann Plast Surg. 1991 Jun;26(6):544-50. doi: 10.1097/00000637-199106000-00008.
Several experimental studies have demonstrated that granulocytes have an important role in causing the necrosis of ischemic tissue by capillary plugging and superoxide radical formation. Adenosine is spontaneously released by ischemic cells and inhibits the granulocytic superoxide radical formation. 5-Aminoimidazole-4-carboxamide riboside, a naturally occurring by-product in purine biosynthesis, stimulates the release of ischemic cell adenosine and indirectly blocks the granulocyte-induced tissue necrosis. 5-Aminoimidazole-4-carboxamide riboside (10-500 mg/kg) was administered intraperitoneally in a blinded fashion once (single dose, 30 minutes before surgery) or twice (double dose, 30 minutes before and 5.5 hours after surgery) in groups of rats. The controls received intraperitoneal saline solution in the same fashion. Each rat underwent the elevation of a caudally based random skin flap. The flap viability was determined in a blinded fashion on the seventh post-operative day and statistically compared by Fisher's exact test. When 300 or 500 mg/kg of 5-aminoimidazole-4-carboxamide riboside was given as a single dose, the mean percentage of rat skin flap necrosis (19.4% +/- 3.1% and 19.6% +/- 4.2%, respectively) was lower but not significantly different from that of the control group of rats (29.3% +/- 2.7%) (p less than 0.08). Additionally, two doses of 500 mg/kg of 5-aminoimidazole-4-carboxamide riboside yielded a mean percentage of rat skin flap necrosis (12.24% +/- 4.58%) much lower (21.68% +/- 3.18%) than that of the control group of rats (p = 0.056). Our blinded fashion study demonstrated an almost statistically significant reduction of random skin flap distal necrosis after intraperitoneal injection of high doses of 5-aminoimidazole-4-carboxamide riboside.(ABSTRACT TRUNCATED AT 250 WORDS)
多项实验研究表明，粒细胞通过毛细血管阻塞和超氧自由基的形成，在导致缺血组织坏死方面发挥着重要作用。腺苷由缺血细胞自发释放，并抑制粒细胞超氧自由基的形成。5-氨基咪唑-4-甲酰胺核苷是嘌呤生物合成过程中天然产生的副产物，它能刺激缺血细胞释放腺苷，并间接阻止粒细胞诱导的组织坏死。将5-氨基咪唑-4-甲酰胺核苷（10 - 500毫克/千克）以盲法腹腔注射给大鼠组，一次（单剂量，手术前30分钟）或两次（双剂量，手术前30分钟和手术后5.5小时）。对照组以相同方式接受腹腔生理盐水溶液。每只大鼠都进行了尾部基底随机皮瓣的掀起。在术后第七天以盲法确定皮瓣活力，并通过Fisher精确检验进行统计学比较。当单剂量给予300或500毫克/千克的5-氨基咪唑-4-甲酰胺核苷时，大鼠皮瓣坏死的平均百分比（分别为19.4%±3.1%和19.6%±4.2%）较低，但与大鼠对照组（29.3%±2.7%）相比无显著差异（p小于0.08）。此外，两剂500毫克/千克的5-氨基咪唑-4-甲酰胺核苷产生的大鼠皮瓣坏死平均百分比（12.24%±4.58%）比大鼠对照组（21.68%±3.18%）低得多（p = 0.056）。我们的盲法研究表明，腹腔注射高剂量的5-氨基咪唑-4-甲酰胺核苷后，随机皮瓣远端坏死几乎在统计学上有显著减少。（摘要截短于250字）
