Lohman R, Yowell R, Barton S, Araneo B, Siemionow M
Division of Plastic and Reconstructive Surgery, University of Utah Medical Center, School of Medicine, Salt Lake City, USA.
J Trauma. 1997 Jan;42(1):74-80. doi: 10.1097/00005373-199701000-00013.
This study evaluated the potential for dehydroepiandrosterone (DHEA) to protect skeletal muscle from reperfusion injury using intravital microscopic observations of isolated rat cremaster muscle flaps. The flaps were subjected to warm ischemia followed by reperfusion in three groups of rats. In group 1 (control, n = 14), muscle flaps were subjected to 6 hours of ischemia and then evaluated after either 90 minutes (n = 8) or 24 hours (n = 6) of reperfusion. Group 2 animals (propylene glycol pretreatment, n = 8) were pretreated with a propylene glycol vehicle, then underwent 6 hours of ischemia and were evaluated after 90 minutes reperfusion. Group 3 animals (DHEA pretreatment, n = 12) were pretreated with DHEA dissolved in propylene glycol, subjected to 6 hours of ischemia, and then evaluated after either 90 minutes (n = 6) or 24 hours (n = 6) of reperfusion. Red blood cell velocity in the flap's main arteriole, functional capillary density, venular constriction index (the ratio of internal to external diameter of postcapillary venules), and microemboli formation were measured. Muscle samples were evaluated by electron microscopy. Control animals showed a 61% reduction in red blood cell velocity (p < 0.05) accompanied by a 69% reduction in functional capillary density (p < .05) acutely and total cessation of flow by 24 hours. No differences between control and propylene glycol treated animals were noted. In DHEA-pretreated animals, reflow occurred in 100% of the flaps, there was a temporary 39% reduction (p < 0.05) in functional capillary density, and all flaps remained viable at 24 hours. In this study, DHEA pretreatment markedly improved muscle flap microcirculatory hemodynamics and protected flaps against ischemia/reperfusion injury.
本研究利用对分离的大鼠提睾肌皮瓣进行活体显微镜观察，评估脱氢表雄酮（DHEA）保护骨骼肌免受再灌注损伤的潜力。将三组大鼠的肌皮瓣进行热缺血然后再灌注。在第1组（对照组，n = 14）中，肌皮瓣经历6小时缺血，然后在再灌注90分钟（n = 8）或24小时（n = 6）后进行评估。第2组动物（丙二醇预处理组，n = 8）用丙二醇载体进行预处理，然后经历6小时缺血，并在再灌注90分钟后进行评估。第3组动物（DHEA预处理组，n = 12）用溶解于丙二醇的DHEA进行预处理，经历6小时缺血，然后在再灌注90分钟（n = 6）或24小时（n = 6）后进行评估。测量皮瓣主要小动脉中的红细胞速度、功能性毛细血管密度、微静脉收缩指数（毛细血管后微静脉内径与外径之比）和微栓子形成情况。通过电子显微镜对肌肉样本进行评估。对照动物急性时红细胞速度降低61%（p < 0.05），同时功能性毛细血管密度降低69%（p < 0.05），到24小时血流完全停止。未观察到对照组和丙二醇处理组动物之间存在差异。在DHEA预处理的动物中，100%的皮瓣出现再灌注，功能性毛细血管密度暂时降低39%（p < 0.05），并且所有皮瓣在24小时时仍保持存活。在本研究中，DHEA预处理显著改善了肌皮瓣的微循环血流动力学，并保护皮瓣免受缺血/再灌注损伤。
